Cause Of Chronic Hypertension Research Articles

The Relationship Between Medication Compliance And The Incidence Of Hypertension Crisis In RSUD. Haji Makassar

A hypertension crisis is an acute complication characterized by a severe increase in blood pressure, generally occurring ≥ 180/120 mmHg. Risk factors for hypertension generally occur due to a history of disease in the family, and age factors as factors that cannot be modified. An unhealthy lifestyle, including consuming alcohol, uncontrolled hypertension, or compliance to taking antihypertension drugs, is a modifiable factor but is often the cause of chronic hypertension to lead to a hypertension crisis. The purpose of this study is to determine the relationship between medication compliance to the incidence of hypertension crisis in hospitals. Makassar Hajj. This study used a cross-sectional research design with a total sampling technique of 34 respondents. This research was carried out in the treatment room of RSUD Haji Makassar. From the results of the study, it can be concluded that compliance to taking medication is associated with the incidence of emergency hypertension with a value of p = 0.008, OR = 112; the more obedient to taking antihypertension drugs, the less likely people with hypertension are to experience hypertension emergencies.

New insights into sodium transport regulation in the distal nephron: Role of G-protein coupled receptors.

The renal handling of Na(+) balance is a major determinant of the blood pressure (BP) level. The inability of the kidney to excrete the daily load of Na(+) represents the primary cause of chronic hypertension. Among the different segments that constitute the nephron, those present in the distal part (i.e., the cortical thick ascending limb, the distal convoluted tubule, the connecting and collecting tubules) play a central role in the fine-tuning of renal Na(+) excretion and are the target of many different regulatory processes that modulate Na(+) retention more or less efficiently. G-protein coupled receptors (GPCRs) are crucially involved in this regulation and could represent efficient pharmacological targets to control BP levels. In this review, we describe both classical and novel GPCR-dependent regulatory systems that have been shown to modulate renal Na(+) absorption in the distal nephron. In addition to the multiplicity of the GPCR that regulate Na(+) excretion, this review also highlights the complexity of these different pathways, and the connections between them.

Abstract 441: Rgs5 Controls Myogenic Responses of Vascular Smooth Muscle Cells

Contraction of vascular smooth muscle cells (VSMCs) in response to an increase in blood pressure is pivotal for maintaining blood flow and constitutes both consequence and cause of chronic hypertension. While a plethora of contraction-mediating mechanisms has been delineated, not much is known about molecular determinants regulating the responses of VSMCs to an increase in wall stress or biomechanical stretch. In this context, we reported that conditional ablation of Junb - a subunit of the transcription factor AP-1 (activator protein 1) - interferes with the expression of myosin light chain 9 and consequently impaired myogenic responses of arteries. We hypothesized that the arterial circumferential wall stress is increased under these conditions which may influence the VSMC phenotype and vessel wall architecture. In fact, Junb-deficient arteries showed structural remodeling as evidenced by a ~2-3-fold decrease in collagen type I and IV content (n=5, p<0.05). cDNA microarray analyses revealed that expression of regulator of G-protein signaling 5 (RGS5) was up-regulated in VSMCs (~6-fold, n=4, p<0.001) isolated from Junb-deficient arteries which was confirmed in vivo but not mediated by AP-1. However, elevation of wall stress by volume-induced hypertension in vivo or exposure of VSMCs to biomechanical stretch in vitro was sufficient to trigger RGS5 expression (3-fold, n=3, p<0.05). Overexpression of this regulator activates RhoA and enhanced stretch-induced responses of VSMCs such as stress fiber formation while its knockdown showed opposite effects. In line with this, RGS5-deficient arteries show an impaired pressure-mediated constriction (n=8, p<0.05) and both the hypertension-induced increase in diastolic blood pressure as well as structural remodeling of the arterial vessel wall were significantly attenuated in RGS5-deficient mice. Collectively, these findings indicate that biomechanical stretch mediates the expression of RGS5 in VSMCs to enhance stretch-dependent responses as a prerequisite for adequate adaptive vascular remodeling processes. This mechanism may establish RGS5 as a promising target for future strategies to combat, e.g. the deleterious consequences of arterial hypertension such as arterial stiffening.

Does Kidney Disease Cause Hypertension?

Hypertension complicates most cases of chronic kidney disease. While the prevalence and severity of hypertension increase as glomerular filtration rate falls, hypertension is often observed in patients with structural kidney disease while renal function is normal, in particular those with polycystic kidney disease or proteinuric glomerular diseases. On the other hand, even severe reductions in renal function may not result in hypertension, especially if there is effective control of extracellular fluid volume. Recent clinical and experimental data indicate that proteinuria may mediate sodium retention and hypertension via plasmin-mediated activation of the epithelial sodium channel. Current evidence supports the notion that chronic kidney disease is a cause of chronic hypertension, even in the absence of detectable changes in glomerular filtration rate.

Analysis of renal hemodynamics and pressure‐natriuresis in Dahl salt‐sensitive rats

Analysis of data on blood flow regulation, filtration, and urine output in Dahl S rats fed on high‐salt (hypertensive) and low‐salt (prehypertensive) diets using simple mathematical models of renal blood flow regulation, glomerular filtration, and solute transport in a nephron reveals the minimal differences between the hypertensive and prehypertensive cases necessary to explain the observed data. It is determined that an increase in renal afferent arterial resistance is able to explain the qualitative differences in observed flows, filtration rates, and glomerular pressure as well as the shift in the pressure‐natriuresis and pressure‐diuresis relationships in animals fed on high compared to low salt diets. Model analysis predicts a decrease in the effective sodium pumping rate in the ascending limb of the loop of Henle in high‐salt fed animals compared to low‐salt fed controls. The finding that a change in afferent arterial tone can explain differences in renal physiological function in high‐salt versus low‐salt fed Dahl S rats suggests the novel hypothesis that, if a shift in the pressure‐natriuresis relationship is the primary cause of elevated arterial pressure in high‐salt fed Dahl S rats, then the primary cause of chronic hypertension in the Dahl S rat is an increase in renal afferent arterial resistance.

Mechanisms of pressure-diuresis and pressure-natriuresis in Dahl salt-resistant and Dahl salt-sensitive rats

BackgroundData on blood flow regulation, renal filtration, and urine output in salt-sensitive Dahl S rats fed on high-salt (hypertensive) and low-salt (prehypertensive) diets and salt-resistant Dahl R rats fed on high-salt diets were analyzed using a mathematical model of renal blood flow regulation, glomerular filtration, and solute transport in a nephron.ResultsThe mechanism of pressure-diuresis and pressure-natriuresis that emerges from simulation of the integrated systems is that relatively small increases in glomerular filtration that follow from increases in renal arterial pressure cause relatively large increases in urine and sodium output. Furthermore, analysis reveals the minimal differences between the experimental cases necessary to explain the observed data. It is determined that differences in renal afferent and efferent arterial resistances are able to explain all of the qualitative differences in observed flows, filtration rates, and glomerular pressure as well as the differences in the pressure-natriuresis and pressure-diuresis relationships in the three groups. The model is able to satisfactorily explain data from all three groups without varying parameters associated with glomerular filtration or solute transport in the nephron component of the model.ConclusionsThus the differences between the experimental groups are explained solely in terms of difference in blood flow regulation. This finding is consistent with the hypothesis that, if a shift in the pressure-natriuresis relationship is the primary cause of elevated arterial pressure in the Dahl S rat, then alternation in how renal afferent and efferent arterial resistances are regulated represents the primary cause of chronic hypertension in the Dahl S rat.

17α-Hydroxylase deficiency; a rare cause of chronic hypertension

We demonstrate a case with 17α-hydroxylase deficiency that presented in an unusual way. The steroid metabolism and diagnostic procedures are discussed.

Hypertension and arteriolar sclerosis of the kidney, pancreas, adrenal gland, and liver.

Replicate slides of autopsy specimens (kidney, pancreas, adrenal glands, and liver) from 66 hospital patients who had lengthy outpatient records of their blood pressure levels were randomized and graded blindly for the severity of hypertensive fibroproliferative-mediodegeneration lesions of arterioles (arplasia). For all four tissues, the severity of lesions correlated significantly with the level of the blood pressure. Between blood pressure and lesions the correlation coefficient was significantly smaller (P Less Than 0.01) for liver and adrenal than for kidney. The correlation coefficient was also smaller for pancreas than for kidney, but the statistical significance of the difference (0.3 Greater Than P Greater Than 0.2) was not conclusive. The results tend to confirm the conclusions of the classic 1937 report of Moritz and Oldt, adding strength to their generalization that "Arteriolar sclerosis is the most common cause of chronic hypertension."

CONFERENCE on the role of the renal pressor system in maintenance of experimental renal hypertension.

The hypothetical presence of increased circulating renin or hypertensin in chronic renal hypertension was debated; eventually it was agreed that methods were too insensitive for accurate assay. Pressor amounts of infused renin could not be detected by some methods of bioassay (Dr. Wakerlin). Hypertensinase activity in blood may destroy the end product before the assay can be performed (Dr. Blaquier). Perhaps rapid tissue removal from circulating blood may account for the inadequacy of the results (Dr. Skeggs). Previous experiments to detect these substances in circulating hypertensive blood have been indecisive (Dr. Braun-Menéndez) or only weakly positive (Drs. Goldblatt and Skeggs) and the clear-cut depressor effects of antirenin might act on a hypothetical nonpressor action of renin (Dr. Wakerlin). Dr. Helmer commented on the sustained pressor substance found in renal vein blood of hypertensive rats. Dr. Grollman believed chronic renal hypertension to be due to interference with an essential function of the kidney which in the normal animal prevents the blood pressure from rising. The failure of the blood pressure to rise when the kidneys from renal hypertensive dogs were perfused in situ by normotensive recipients was again discussed by Drs. Surtshin, Goldblatt and Grollman, and the possible fallacies involved in reasoning from such acute experiments were brought out. The nature of the stimulus to renin release was discussed again by Dr. Kolff. Non pulsatile flow was probably not a requirement (Dr. Kolff), nor was renal ischemia (Dr. Wakerlin), but some alteration in renal function seemed to be necessary (Dr. Goldblatt). Dr. Wakerlin and Dr. Rodbard advocated, respectively, the view that the primary stimulus might be the volume pulse or the transmural pressure in the renal arterial bed. An objection to renin as the cause of chronic hypertension based on tachyphylaxis experiments was raised by Dr. Findley. Dr. Goldblatt denied the presence of true tachyphylaxis and was supported by Drs. Helmer and Wakerlin. Dr. McCubbin suggested it might occur only with cruder preparations of renin, and Dr. Braun-Menéndez theorized that receptor sites might be occupied for a time after restoration of normal blood pressure, thus giving rise to a transient tachyphylaxis. Dr. Bumpus supported this explanation by reporting that a pressor response to crude angiotonin can sometimes not be maintained, while the response to pure angiotonin is persistent. Considerable discussion ensued between Drs. Goldblatt and Grollman concerning the mechanism of blood pressure reduction by removal of a single ischemic kidney. The human renal biopsy and autopsy studies suggesting the primacy of renal arteriolosclerosis in human hypertension were reviewed by Dr. Goldblatt.