Pathophysiology Of Hypertension Research Articles

Revisiting resistant hypertension in kidney disease.

As compared to controlled or uncontrolled hypertension, resistant hypertension in patients with chronic kidney disease (CKD) poses a significantly increased healthcare burden due to greater target end-organ damage including cardiovascular disease and CKD progression. Patients with CKD have two to three times higher risk of developing resistant hypertension. True resistant hypertension needs to be distinguished from apparent treatment resistant hypertension (aTRH); however, it is usually not possible in epidemiological studies. Moreover, impact of contemporary guidelines changes in the target blood pressure (BP) goal to less than 130/80 mmHg remains to be determined. Up to half of patients with CKD meet aTRH criteria using 2017 ACC/AHA target BP less than 130/80 mmHg. Excess sodium retention in extracellular and tissue compartment remains the cornerstone cause of resistance to the treatment in CKD. Maximizing and optimizing the diuretic regimen in addition to dietary sodium restriction plays a critical role in these patients. Management requires a trustworthy provider-patient relationship facilitating identification and intervention for the barriers restricting the uptake of lifestyle modifications and medications. Recently, renal denervation has been approved and many other novel agents are on the horizon for treatment of true resistant hypertension associated with CKD. This review discusses the latest in the pathophysiology, definition, identification and treatment strategies of resistant hypertension in individuals with CKD. Further investigations are required to identify the prevalence, future implication and treatment outcome data for true resistant hypertension associated with CKD.

Noninvasive Pressure-Volume Loops Predict Major Adverse Cardiac Events in Heart Failure With Reduced Ejection Fraction

BackgroundHeart failure with reduced ejection fraction (HFrEF) is characterized by ventricular remodeling and impaired myocardial energetics. Left ventricular pressure-volume (PV) loop analysis can be performed noninvasively using cardiovascular magnetic resonance (CMR) imaging to assess cardiac thermodynamic efficiency. ObjectivesThe aim of the study was to investigate whether noninvasive PV loop parameters, derived from CMR, could predict major adverse cardiac events (MACE) in HFrEF patients. MethodsPV loop parameters (stroke work, ventricular efficiency, external power, contractility, and energy per ejected volume) were computed from CMR cine images and brachial blood pressure. The primary endpoint was MACE (cardiovascular death, heart failure (HF) hospitalization, myocardial infarction, revascularization, ventricular tachycardia/fibrillation, heart transplantation, or left ventricular assist device implantation within 5 years). Associations between PV loop parameters and MACE were evaluated using multivariable Cox regression. ResultsA total of 164 HFrEF patients (left ventricular ejection fraction ≤40%, age 63 [IQR: 55-70] years, 79% male) who underwent clinical CMR examination between 2004 and 2014 were included. Eighty-eight patients (54%) experienced at least 1 MACE after an average of 2.8 years. Unadjusted models demonstrated a significant association between MACE and all PV loop parameters (P < 0.05 for all), HF etiology (P < 0.001), left ventricular ejection fraction (P = 0.003), global longitudinal strain (P < 0.001), and N-terminal prohormone of brain natriuretic peptide level (P = 0.001). In the multivariable Cox regression analysis adjusted for age, sex, hypertension, diabetes, and HF etiology, ventricular efficiency was associated with MACE (HR: 1.04, 95% CI: 1.01-1.08, per-% decrease, P = 0.01). ConclusionsVentricular efficiency, derived from noninvasive PV loop analysis from standard CMR scans, is associated with MACE in patients with HFrEF.

Case Report of a Large Endometrioma Precipitating a Hypertensive Emergency [ID 2683395

INTRODUCTION: This is a rare case of a 25-cm endometrioma in a woman who presented in a hypertensive emergency. The hypertension was believed to be secondary to the mass effect of the endometrioma on renal vasculature. METHODS: A 20-year-old female presented to the ED with diffuse abdominal pain, severe hypertension (190/121), and acute kidney injury (AKI) (Cr 2.4, GFR 38). At presentation, management of hypertension required intravenous hydralazine and adequate pain control. The workup included an abdominal CT that revealed a large 25×18×12-cm cystic mass. The mass was suspected to have a significant mass-effect on adjacent structures that caused bilateral hydroureteronephrosis secondary to distal ureteral compression. Management of this case began with the placement of bilateral nephrostomy tubes to improve renal function. The pelvic mass was removed with a minimally invasive robotic approach. The patient had an uneventful postoperative course with normalization of blood pressure and resolution of the AKI. Pathology confirmed the diagnosis of endometriosis. Prior to the removal of nephrostomy tubes, a nephrostogram was performed, which demonstrated appropriate drainage bilaterally. At 1 year follow-up, the patient was asymptomatic and was able to conceive. This case report was IRB-exempt. CONCLUSION: A multidisciplinary approach to the management of endometriosis is often warranted as it may affect organs outside of the reproductive system. In this case, the etiology of hypertension is believed to be due to mass effect of the cyst on the renal arteries. Low renal perfusion activates the renin–angiotensin–aldosterone system, releasing Angiotensin II and aldosterone, causing systemic vasoconstriction and secondary hypertension. In this case, a minimally invasive approach to remove the mass and ureterolysis resulted in the resolution of the pelvic pain, AKI, and normalization of blood pressure.

Addressing the enigma of treating heart failure with preserved ejection fraction with P2X3 receptor antagonism

Heart failure with preserved ejection fraction (HFpEF) is a major health burden and a primary cause of death globally, yet there remains no curative treatment. Previous studies have indicated an important role for P2X3 receptors (P2X3R) in mediating high levels of sympathetic drive in hypertension (1). Given the high sympathetic drive in HFpEF(2), we investigated whether P2X3R antagonism would improve this condition. We tested the hypotheses that in HFpEF, P2X3R activation causes high levels of blood pressure and excessive vasoconstriction in the hindlimb vasculature during exercise. Following unilateral renal artery clipping, an ovine model of HFpEF was established in female sheep displaying hypertension and diastolic dysfunction. A sham-operated group acted as a control. Mean arterial pressure (MAP), heart rate (HR), and hindlimb blood flow (HLBF) were recorded before and during treadmill exercise, and the effect of either a P2X3R antagonist (L227, 10mg/kg) or vehicle was assessed. The clipping of one renal artery increased MAP (91±5 vs. 131±6, p≤0.05). The administration of the P2X3R antagonist reduced both MAP (-6±7 mmHg, p≤0.05) and HR (-6±6 bpm, p&lt;0.05) in HFpEF sheep but no effect in sham-operated animals. HLBF during exercise was attenuated in the HFpEF model compared to sham-operated sheep (an increase of 2±1 vs. 4±2 L/min, respectively, p&lt;0.05). Importantly, P2X3R blockade improved the change in HLBF during exercise from 1±0.1 to 2±0.4 L/min in HFpEF sheep, but there was no change in the sham-operated animals. There was no change in the MAP or HR response to the exercise with the P2X3R blockade. P2X3R plays a role in the aetiology of hypertension and in the attenuation of HLBF responses during exercise in HFpEF. P2X3R antagonism may provide a novel target to alleviate symptoms of HFpEF and improve exercise tolerance through increased HLBF. 1. Pijacka W, Moraes DJ, Ratcliffe LE, Nightingale AK, Hart EC, da Silva MP, Machado BH, McBryde FD, Abdala AP, Ford AP and Paton JFR. Purinergic receptors in the carotid body as a new drug target for controlling hypertension. Nature medicine 22: 1151-1159, 2016. 2. Seravalle G, Quarti-Trevano F, Dell’Oro R, Gronda E, Spaziani D, Facchetti R, Cuspidi C, Mancia G, and Grassi G. Sympathetic and baroreflex alterations in congestive heart failure with preserved, midrange and reduced ejection fraction. Journal of Hypertension 37: 443-448, 2019. Health Research Council of New Zealand and Sidney Taylor Trust. This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

MICROWAVE TISSUE DIGESTION AND FLAME ATOMIC ABSORPTION SPECTROSCOPY FOR MEASURING TISSUE SODIUM CONTENT IN HYPERTENSIVE AND CARDIOVASCULAR RISK PATIENTS

Objective: Skin sodium accumulation has been demonstrated in hypertensive patients and may contribute to the pathophysiology of hypertension. Various methods are available for measuring tissue sodium content. However, the accuracy and reproducibility of these methods remain unknown. Dry ashing is the most used digestion method, but is expensive, time consuming and has a risk of incomplete digestion. This study compared microwave digestion, dry ashing, and two electrolyte quantification methods for quantifying tissue sodium and potassium. Design and method: We compared microwave digestion (Ethos LEAN Compact Microwave Digestion System, Milestone SRL) and dry ashing (Nabertherm S27) as sample preparation methods, and flame atomic absorption spectroscopy (FAAS, Model 425 Flame Photometer, Sherwood Scientific) and inductively coupled plasma optical emission spectrometry (ICP-OES, Varian 720-ES, Varian Inc.) as electrolyte quantification methods. Skin and muscle samples were obtained from rats and mice, and human skin samples were used. Tissues biopsies were cut in three pieces and digested separately. The methods were compared using interclass correlation coefficient (ICC) and Bland-Altman analysis. The third piece of tissue was microwave-digested by another operator to test inter-operator reproducibility by calculating the ICC and absolute overall mean difference. Results: With microwave digestion and FAAS median (IQR) human skin concentration was 114.8 (99.2-157.0, n=12) mmol/L, confirming tissue sodium storage. When including all tissues, FAAS and ICP-OES showed high agreement for sodium (ICC 0.98, bias -0.00008 mmol/g, n=141 and potassium (ICC 0.98, bias -0.005 mmol/g, n=141). Microwave digestion and ashing showed agreement for sodium (ICC 0.93, bias -0.002 mmol/g, n=61) and potassium (ICC 0.93, bias -0.02 mmol/g, n=61). The inter-operator agreement was good for sodium (ICC 0.95, absolute mean difference (SD) 0.044 mmol/g (0.073), n=70) and potassium (ICC 0.96, absolute mean difference (SD) 0.031 mmol/g (0.032), n=70). Conclusions: Microwave digestion with FAAS is a reliable and consistent method for sodium and potassium trace analysis in animal and human tissues compared to ashing and ICP-OES, respectively. This method showed more quantification of cations than the most frequently reported method, representing an easier, and less time-consuming way to quantify tissue sodium in hypertension and cardiovascular research.

Systemic Hormonal Unloading (SHU) in Secondary Hypertension: Addressing the Long-Term Adverse Cardiovascular Outcomes

Excess hormone production from adrenal tumors caused by primary hyperaldosteronism or pheochromocytoma are common etiologies for secondary hypertension. Studies have shown that sustained long-term circulating hormones in excess affect the blood vessels and cardiac structures. Inflammation of cardiomyocytes leads to fibrosis and eventual cardiomyopathy and is clinically presented as arrhythmia, nonfatal myocardial infarction, heart failure, or even death. The tissue changes and/or impaired cardiac function are reversible if early diagnosis and removal of the adrenal tumor by unilateral adrenalectomy is done. However, the condition becomes challenging if the adrenal lesions are bilateral. This article introduces the concept of systemic hormonal unloading and will discuss the philosophy of quality of life in managing bilateral adrenal disease. Keywords: systemic hormonal unloading, secondary hypertension, primary hyperaldosteronism, pheochromocytoma, bilateral adrenal venous sampling, cardiovascular adverse outcomes, quality of life

Immune mechanisms in the pathophysiology of hypertension.

Hypertension is a leading risk factor for morbidity and mortality worldwide. Despite current anti-hypertensive therapies, most individuals with hypertension fail to achieve adequate blood pressure control. Moreover, even with adequate control, a residual risk of cardiovascular events and associated organ damage remains. These findings suggest that current treatment modalities are not addressing a key element of the underlying pathology. Emerging evidence implicates immune cells as key mediators in the development and progression of hypertension. In this Review, we discuss our current understanding of the diverse roles of innate and adaptive immune cells in hypertension, highlighting key findings from human and rodent studies. We explore mechanisms by which these immune cells promote hypertensive pathophysiology, shedding light on their multifaceted involvement. In addition, we highlight advances in our understanding of autoimmunity, HIV and immune checkpoints that provide valuable insight into mechanisms of chronic and dysregulated inflammation in hypertension.

Hypoxic perfusion of pulmonary arterial vasa vasorum increases pulmonary arterial pressure.

The pathophysiology of pulmonary hypertension (PH) is not fully understood. Here, we tested the hypothesis that hypoxic perfusion of the vasa vasorum of the pulmonary arterial (PA) wall causes PH. Young adult pig lungs were explanted and placed into a modified ex vivo lung perfusion unit (organ care system, OCS) allowing the separate adjustment of parameters for mechanical ventilation, as well as PA perfusion and bronchial arterial (BA) perfusion. The PA vasa vasorum are branches of the BA. The lungs were used either as the control group (n = 3) or the intervention group (n = 8). The protocol for the intervention group was as follows: normoxic ventilation and perfusion (steady state), hypoxic BA perfusion, steady state, and hypoxic BA perfusion. During hypoxic BA perfusion, ventilation and PA perfusion maintained normal. Control lungs were kept under steady-state conditions for 105 min. During the experiments, PA pressure (PAP) and blood gas analysis were frequently monitored. Hypoxic perfusion of the BA resulted in an increase in systolic and mean PAP, a reaction that was reversible upon normoxic BA perfusion. The PAP increase was reproducible during the second hypoxic BA perfusion. Under control conditions, the PAP stayed constant until about 80 min of the experiment. In conclusion, the results of the current study prove that hypoxic perfusion of the vasa vasorum of the PA directly increases PAP in an ex situ lung perfusion setup, suggesting that PA vasa vasorum function and wall ischemia may contribute to the development of PH.NEW & NOTEWORTHY Hypoxic perfusion of the vasa vasorum of the pulmonary artery directly increased pulmonary arterial pressure in an ex vivo lung perfusion setup. This suggests that the function of pulmonary arterial vasa vasorum and wall ischemia may contribute to the development of pulmonary hypertension.

MFAP4-Deficiency Aggravates Age-Induced Changes in Resistance Artery Structure, While Ameliorating Hypertension.

Abnormalities of resistance arteries may play essential roles in the pathophysiology of aging and hypertension. Deficiency of the vascular extracellular matrix protein MFAP4 (microfibrillar-associated protein 4) has previously been observed as protective against aberrant arterial remodeling. We hypothesized that MFAP4-deficiency would reduce age- and hypertension-dependent arterial changes in extracellular matrix composition and stiffening. Mesenteric arteries were isolated from old (20-23 months) littermate Mfap4+/+ and Mfap4-/- mice, and 2-photon excitation microscopy imaging was used to quantify elastin and collagen volumes and dimensions in the vascular wall. Ten-week-old littermate Mfap4+/+ and Mfap4-/- mice were subjected to 20 days of continuous Ang II (angiotensin II) infusion and hypertension was monitored using invasive blood pressure measurements. Arterial stiffness, responses to vascular constrictors, and myogenic tone were monitored using wire- or pressure-myography. Collagen contents were assessed by Western blotting. MFAP4-deficiency significantly increased collagen volume and elastin fragmentation in aged mesenteric arteries without affecting arterial stiffness. MFAP4-deficient mice exhibited reduced diastolic pressure in Ang II-induced hypertension. There was no significant effect of MFAP4-deficiency on mesenteric artery structural remodeling or myogenic tone, although collagen content in mesenteric arteries was tendentially increased in hypertensive Mfap4+/+ mice relative to Mfap4-/- mice. Increased efficacy of vasoconstrictors (phenylephrine, thromboxane) and reduced stiffness were observed in Ang II-treated Mfap4-/- mouse mesenteric arteries in ex vivo myography recordings. MFAP4-deficiency reduces the elastin/collagen ratio in the aging resistance artery without affecting arterial stiffness. In contrast, MFAP4-deficiency reduces the stiffness of resistance arteries and ameliorates Ang II-induced hypertension.

Fundus Bleeding

Abstract Fundus bleeding, commonly known as retinal haemorrhage, is a significant ocular manifestation associated with various systemic and ocular conditions. This abstract provides a comprehensive overview of the pathogenesis, diagnosis and management strategies of fundus bleeding. The abstract begins by discussing the underlying pathophysiology of fundus bleeding, which involves the rupture of retinal blood vessels leading to the extravasation of blood into the retinal layers. It highlights the diverse aetiologies of retinal haemorrhage, including trauma, vascular diseases, hypertension, diabetes, blood dyscrasias and ocular conditions such as retinal vein occlusion and macular degeneration. The manuscript further delves into the diagnostic modalities used to assess fundus bleeding, including fundus examination, optical coherence tomography (OCT), fluorescein angiography (FA) and fundus photography. It emphasizes the importance of accurate diagnosis to identify the underlying cause and guide appropriate management. The management strategies for fundus bleeding are discussed, considering both the underlying aetiology and severity of the haemorrhage. This includes conservative approaches, such as observation and control of systemic risk factors, as well as specific interventions like antivascular endothelial growth factor (anti-VEGF) therapy, laser photocoagulation and vitrectomy. In conclusion, this abstract provides a comprehensive overview of the pathogenesis, diagnosis and management of fundus bleeding or retinal haemorrhage. It serves as a valuable resource for clinicians and researchers involved in the care of patients with retinal haemorrhage, aiding in the understanding of its multifactorial aetiology and guiding evidence-based management strategies for improved visual outcomes.

Foundations of the Diagnosis and Management of Idiopathic Intracranial Hypertension and Pulsatile Tinnitus

Venous sinus stenosis has garnered increasing academic attention as a potential etiology of idiopathic intracranial hypertension (IIH) and pulsatile tinnitus (PT). The complex anatomy of the cerebral venous sinuses and veins plays a crucial role in the pathophysiology of these conditions. Venous sinus stenosis, often found in the superior sagittal or transverse sinus, can lead to elevated intracranial pressure (ICP) and characteristic IIH symptoms. Stenosis, variations in dural venous anatomy, and flow dominance patterns contribute to aberrant flow and subsequent PT. Accurate imaging plays a vital role in diagnosis, and magnetic resonance (MR) venography is particularly useful for detecting stenosis. Management strategies for IIH and PT focus on treating the underlying disease, weight management, medical interventions, and, in severe cases, surgical or endovascular procedures. Recently, venous sinus stenting has gained interest as a minimally invasive treatment option for IIH and PT. Stenting addresses venous sinus stenosis, breaking the feedback loop between elevated ICP and stenosis, thus reducing ICP and promoting cerebrospinal fluid outflow. The correction and resolution of flow aberrances can also mitigate or resolve PT symptoms. While venous sinus stenting remains an emerging field, initial results are promising. Further research is needed to refine patient selection criteria and evaluate the long-term efficacy of stenting as compared to traditional treatments.

From Sugar Spikes to Pressure Peaks: Navigating the World of Diabetes, Hypertension, Obesity, and Kidney Health.

Diabetes, hypertension, obesity, and chronic kidney disease (CKD) are major public health challenges globally, contributing significantly to morbidity and mortality. The co-occurrence and interplay among these conditions exacerbate health outcomes, highlighting the need for an integrated understanding and approach to management. This narrative review aims to explore the complex relationships between diabetes, hypertension, obesity, and CKD, elucidating their collective impact on health. It discusses the epidemiological trends, underlying pathophysiological mechanisms, genetic predispositions, current treatment strategies, and the future direction of research and therapy. An extensive review of current literature was conducted, focusing on the epidemiology, pathophysiology, risk factors, diagnosis, and treatment of diabetes, hypertension, obesity, and CKD. Additionally, the review delves into the genetic and molecular biology underlying these conditions, the potential for personalized medicine, and the importance of a multidisciplinary approach to care. The review identifies key areas where these conditions intersect, enhancing disease progression and complicating management. It highlights the role of genetic and environmental factors in disease etiology, the critical need for personalized treatment strategies, and the gaps in current management approaches. Innovations in pharmacotherapy, monitoring technologies, and the potential of pharmacogenomics are discussed as avenues for advancing patient care. Diabetes, hypertension, obesity, and CKD are intricately linked, necessitating an integrated, patient-centered approach to care that goes beyond traditional treatment modalities. Future research should focus on collaborative models and interdisciplinary strategies to address the multifaceted challenges posed by these conditions. Emphasizing personalized medicine and leveraging technological advancements offer promising pathways to improve outcomes and reduce the global health burden of these metabolic disorders.

Management of hypertension in heart transplant recipients: an ongoing conundrum.

Hypertension remains one of the most common clinical problems leading to significant posttransplant complications. This study reviews the pathophysiology of hypertension in the postcardiac transplant phase and provides an update on currently available antihypertensive therapies for heart transplant patients. The true prevalence of hypertension in the heart transplant population remains unknown. Effective blood pressure (BP) control is key to prevent left ventricular remodeling, diastolic dysfunction and stroke. Calcium channel blockers (CCBs) are the most commonly and preferred agents in the early posttransplant phase and may have renal protective effects. Angiotensin-converting enzyme inhibitors (ACEIs), angiotensin receptor blockers (ARBs) can all be used as second line antihypertensive agents and may have a role in preventing other long-term complications such as calcineurin-inhibitor induced nephropathy. Although more data are needed, sodium-glucose co-transporter 2 inhibitors (SGLT2i) appeared to be well tolerated and could be considered especially in the presence of type diabetes and chronic kidney disease. Conversely, angiotensin receptor-neprilysin inhibition (ARNI) have not been studied in the heart transplant population therefore cannot be recommended at this time. Hypertension is very common after heart transplant. Early steroid wean and traditional risk factor modification play an important part in the management of post-heart transplant hypertension. CCB, ACEI, ARB are the preferred antihypertensive agents to improve postcardiac transplant complications. Novel therapies such as SGLT2i appear well tolerated and may have benefits in both BP and glycemic control in heart transplant; however, larger trials are needed.

Association between skin lymphangiogenesis parameters and arterial hypertension status in patients: An observational study.

Recent studies have indicated that the skin lymphatic system and interstitium may play a role in the pathophysiology of arterial hypertension (AH). We aimed to determine whether the set of pathway parameters described previously in rodents would allow for the distinction between hypertensive and normotensive patients. Molecular and histopathological parameters from the skin and blood of patients with AH (AH group, n = 53), resistant AH (RAH group, n = 32) and control (C group, n = 45) were used, and a statistical multivariate bootstrap methodology combining partial least squares-discriminant analysis (PLS-DA) and selectivity ratio (SR) were applied. The C vs RAH model presented the best prediction performance (AUC test = 0.90) and had a sensitivity and specificity of 73.68% and 83.33%, respectively. However, the parameters selected for the C vs AH group model were the most important for the pathway described in the rodent model, i.e., greater density of the skin lymphatic vessels (D2-40 expression) and greater number of macrophages (CD68 expression), higher expression of the messenger ribonucleic acid (mRNA) of nuclear factor of activated T cells 5 (NFAT5), vascular endothelial growth factor C (VEGFC) and podoplanin (PDPN) in the skin, greater concentration of hyaluronic acid (HA) in the skin, and lower serum concentration of VEGF-C. Our study suggests that the NFAT5/VEGF-C/lymphangiogenesis pathway, previously described in rodent studies, may also be present in human HA. Further experiments are needed to confirm our findings.

Targeting Hypertension: A Review on Pathophysiological Factors and Treatment Strategies.

Hypertension is one of the primary causes of cardiovascular diseases and death, with a higher prevalence in low- and middle-income countries. The pathophysiology of hypertension remains complex, with 2% to 5% of patients having underlying renal or adrenal disorders. The rest are referred to as essential hypertension, with derangements in various physiological mechanisms potentially contributing to the development of essential hypertension. Hypertension elevates the risk of cardiovascular disease (CVD) events (coronary heart disease, heart failure, and stroke) and mortality. First-line therapy for hypertension is lifestyle change, which includes weight loss, a balanced diet that includes low salt and high potassium intake, physical exercise, and limitation or elimination of alcohol use. Blood pressure-lowering effects of individual lifestyle components are partially additive, enhancing the efficacy of pharmaceutical treatment. The choice to begin antihypertensive medication should be based on the level of blood pressure and the existence of a high atherosclerotic CVD risk. First-line hypertension treatment includes a thiazide or thiazide-like diuretic, an angiotensin-converting enzyme inhibitor or angiotensin receptor blocker, and a calcium channel blocker. Addressing hypertension will require continued efforts to improve access to diagnosis, treatment, and lifestyle interventions.

Pathophysiology, Diagnosis, and Management of Portal Hypertension in the Pediatric Population

AbstractPortal hypertension is caused by resistance to the portal blood flow, which most commonly occurs in the setting of cirrhosis. Complications of portal hypertension can cause significant morbidity and mortality in the pediatric population. Portal hypertension is diagnosed when the hepatic venous pressure gradient (HVPG) is more than 5 mm Hg, and potential bleeding complications from esophageal and gastric varices are more likely when the HVPG is more than 10 mm Hg. Diagnosis can be made clinically; however, liver biopsy with measurement of the HVPG is ultimately required. The management of portal hypertension in pediatric patients is typically aimed at treatment of the complications. Despite the multiple pharmacologic, endoscopic, surgical, and interventional radiologic management techniques that are available, some pediatric patients will ultimately require liver transplant. Prompt referral is needed in such cases.

Evaluation of Patients Diagnosed with Essential Hypertension in Terms of Mental and Personality Disorders.

Recent studies have suggested a link between hypertension and psychiatric disorders. However, the relationship between hypertension and mental health conditions remains unclear. So in this study, it was aimed to compare the prevalence of psychiatric diseases seen in hypertension patients with the healthy group. Psychiatric interviews were conducted with 104 patients in the hypertension group and 102 participants in the control group. The Sociodemographic and Clinical Data Form, Hamilton Depression Rating Scale (HAM-D), Hamilton Anxiety Rating Scale (HAM-A), Structured Clinical Interview for Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5) Disorders, Structured Clinical Interview for DSM-5-Clinician Version, and DSM-5 Structured Clinical Interview for Personality Disorders were implemented for participants. Patients with hypertension were found to have a significantly higher number of psychiatric disorders compared to the control group (χ 2 = 29.389; P = .001). Statistically significant difference in the diagnosis of severe depression, chronic depression disorder, and specific phobia was discovered between the 2 groups (P < .05). The HAM-A and HAM-D scores were also significantly higher in the hypertension group (P < .001). No statistically significant difference was found between the patient and control groups in terms of the frequency of personality disorders. (χ 2 = 0.045; P = .833). The fact that depression and anxiety symptoms are more common in hypertension patients stands out as a subject that needs further investigation in terms of both the pathophysiology of hypertension. In this regard, since essential hypertension is a serious risky disease for mortality and morbidity on its own, it is critical to conduct psychiatric screening and develop new additional treatments to provide patients with supportive care.

Clinical Correlates of a Nonplexiform Vasculopathy in Patients With a Diagnosis of Idiopathic Pulmonary Arterial Hypertension

The clinical phenotype of idiopathic pulmonary arterial hypertension (IPAH) patients has changed. . Whether or not subgroups of IPAH patients have different vascular phenotypes is a subject of debate. What are the histological patterns and their clinical correlates in patients diagnosed with IPAH or hereditary PAH? In this this cross-sectional registry study lung histology of 50 IPAH patients was qualitatively assessed by two experienced pathologists. In addition, quantitative analysis by means of histopathological morphometry using immunohistochemistry was performed. Histopathological characteristics were correlated with clinical and hemodynamic parameters. In this cohort of 50 IPAH patients, a plexiform vasculopathy was observed in 26/50 (52%) of patients, while 24/50 (48%) patients had a non-plexiform vasculopathy. The non-plexiform vasculopathy was characterized by prominent pulmonary microvascular (arterioles and venules) remodeling and vascular rarefaction. While hemodynamic parameters were comparable in plexiform versus non-plexiform vasculopathy, patients with non-plexiform vasculopathy were older, more often male, had a stronger history of cigarette smoking and lower diffusing capacity for carbon monoxide (DLCO) at diagnosis No mutations in established PAH genes were found in the non-plexiform group. This study reveals different vascular phenotypes within the current spectrum of patients diagnosed with IPAH, separated by clinical characteristics (age, sex, , history of cigarette smoking, and DLCO at diagnosis). Potential differences in underlying pathobiological mechanisms between patients with plexiform and non-plexiform / microvascular disease should be taken into account in future research strategies unravelling the pathophysiology of pulmonary hypertension and developing biology-targeted treatment approaches.

Mesenteric artery smooth muscle cells from hypertensive rats have increased microtubule acetylation.

The dynamic nature of the microtubule network is dependent in part by post-translational modifications (PTMs) - particularly through acetylation, which stabilizes the microtubule network. Whether PTMs of the microtubule network in vascular smooth muscle cells (VSMCs) contribute to the pathophysiology of hypertension is unknown. The aim of this study was to determine the acetylated state of the microtubule network in the mesenteric arteries of spontaneously hypertensive rats (SHR). Experiments were performed on male normotensive rats and SHR mesenteric arteries. Western blotting and mass spectrometry determined changes in tubulin acetylation. Wire myography was used to investigate the effect of tubacin on isoprenaline-mediated vasorelaxations. Isolated cells from normotensive rats were used for scanning ion conductance microscopy (SICM). Mass spectrometry and Western blotting showed that tubulin acetylation is increased in the mesenteric arteries of the SHR compared with normotensive rats. Tubacin enhanced the β-adrenoceptor-mediated vasodilatation by isoprenaline when the endothelium was intact, but attenuated relaxations when the endothelium was denuded or nitric oxide production was inhibited. By pre-treating vessels with colchicine to disrupt the microtubule network, we were able to confirm that the effects of tubacin were microtubule-dependent. Using SICM, we examined the cell surface Young's modulus of VSMCs, but found no difference in control, tubacin-treated, or taxol-treated cells. Acetylation of tubulin at Lys40 is elevated in mesenteric arteries from the SHR. Furthermore, this study shows that tubacin has an endothelial-dependent bimodal effect on isoprenaline-mediated vasorelaxation.

Chronic intermittent hypoxia-induced hypertension: the impact of sex hormones.

Obstructive sleep apnea, a common form of sleep-disordered breathing, is characterized by intermittent cessations of breathing that reduce blood oxygen levels and contribute to the development of hypertension. Hypertension is a major complication of obstructive sleep apnea that elevates the risk of end-organ damage. Premenopausal women have a lower prevalence of obstructive sleep apnea and cardiovascular disease than men and postmenopausal women, suggesting that sex hormones play a role in the pathophysiology of sleep apnea-related hypertension. The lack of protection in men and postmenopausal women implicates estrogen and progesterone as protective agents but testosterone as a permissive agent in sleep apnea-induced hypertension. A better understanding of how sex hormones contribute to the pathophysiology of sleep apnea-induced hypertension is important for future research and possible hormone-based interventions. The effect of sex on the pathophysiology of sleep apnea and associated intermittent hypoxia-induced hypertension is of important consideration in the screening, diagnosis, and treatment of the disease and its cardiovascular complications. This review summarizes our current understanding of the impact of sex hormones on blood pressure regulation in sleep apnea with a focus on sex differences.