Elevated Arterial Blood Pressure Research Articles

Comparative analysis of the persistence of a conditioned passive avoidance reflex in rats with different forms of inherited hypertension

The characteristics of anxiety behavior and reproduction of a conditioned passive avoidance reflex acquired in response to a single combination with an unconditioned aversive stimulus were studied in NISAG rats with inherited stress-sensitive arterial hypertension and spontaneously hypertensive SHR rats. SHR rats were characterized by hyperactive behavior, very low levels of anxiety, and poor reproduction of the conditioned reflex as compared with NISAG and control Wistar and WAG rats. Intermediate-anxiety NISAG rats showed no difficulties in acquiring and subsequently retaining the conditioned reflex. These differences in the ability to undergo single-combination learning in rats with different forms of hypertension suggest that memory processes are independent of elevated arterial blood pressure. The effects of the genetic characteristics of behavior and emotional status of these animals on memory are discussed.

Guanylyl cyclase/natriuretic peptide receptor-A gene disruption causes increased adrenal angiotensin II and aldosterone levels

Disruption of the guanylyl cyclase-A/natriuretic peptide receptor-A (GC-A/NPRA) gene leads to elevated arterial blood pressure and congestive heart failure in mice lacking NPRA. This study was aimed at determining whether Npr1 (coding for GC-A/NPRA) gene copy number affects adrenal ANG II and aldosterone (Aldo) levels in a gene-dose-dependent manner in Npr1 gene-targeted mice. Adrenal ANG II and Aldo levels increased in 1-copy mice compared with 2-copy mice, but decreased in 3-copy and 4-copy mice. In contrast, renal ANG II levels decreased in 1-copy (25%), 3-copy (38%), and 4-copy (39%) mice compared with 2-copy mice. The low-salt diet stimulated adrenal ANG II and Aldo levels in 1-copy (20 and 2,441%), 2-copy (15 and 2,339%), 3-copy (20 and 424%), and 4-copy (31 and 486%) mice, respectively. The high-salt diet suppressed adrenal ANG II and Aldo levels in 1-copy (46 and 29%) and 2-copy (38 and 17%) mice. On the other hand, the low-salt diet stimulated renal ANG II levels in 1-copy (45%), 2-copy (45%), 3-copy (59%), and 4-copy (48%) mice. However, the high-salt diet suppressed renal ANG II levels in 1-copy (28%) and 2-copy (27%) mice. In conclusion, NPRA signaling antagonizes adrenal ANG II and Aldo levels in a gene-dose dependent manner. Increased adrenal ANG II and Aldo levels may play an important role in elevated arterial blood pressure and progressive hypertension, leading to renal and vascular injury in Npr1 gene-disrupted mice.

PHARMACOKINETICS AND PHARMACODYNAMICS OF A NITRIC OXIDE‐RELEASING DERIVATIVE OF ENALAPRIL IN MALE BEAGLES

1. Pharmacological compounds that release nitric oxide (NO) have been useful tools in the evaluation of the broad role of NO in physiopathology and therapeutics. The present study compared the pharmacokinetics and pharmacodynamics of enalapril and an NO-releasing enalapril molecule (NCX899) in conscious male beagles. The effects of both enalapril and NCX899 in the arterial hypertension and bradycardia induced by acute NO inhibition in anaesthetized dogs were also investigated. 2. Dogs received either NCX899 (4 micromol/kg, i.v.) or enalapril (4 micromol/kg, i.v.), after which plasma concentrations of the analytes and metabolites were quantified by liquid chromatography coupled to tandem mass spectrometry (LC-MS/MS). 3. In the NCX899 group, the area under the time-course curve (AUC(0-24h)) was 29.18 +/- 4.72, 229.37 +/- 51.32 and 5159.23 +/- 514.88 microg.h/L for the analytes nitro-enalapril, enalapril and enalaprilat, respectively. In the enalapril group, the AUC(0-24h) was 704.53 +/- 158.86 and 4149.27 +/- 847.30 microg.h/L for the analytes enalapril and enalaprilat, respectively. Statistical analysis of data from both groups showed a significant difference for the analyte enalapril, but not for enalaprilat. Moreover, NCX899 and enalapril were equally effective in inhibiting the activity of serum angiotensin-converting enzyme. 4. In anaesthetized dogs, i.v. administration of the NO synthase (NOS) inhibitor N(G)-nitro-l-arginine methyl ester (l-NAME; 0.1-10 mg/kg) significantly elevated arterial blood pressure, with concomitant bradycardia. The compound NCX899 significantly attenuated both arterial hypertension and bradycardia, whereas enalapril had no significant effect. 5. In conclusion, the present results showed that the NO-releasing derivative of enalapril NCX899 presents a pharmacokinetic/pharmacodynamic relationship similar to its parent compound enalapril. Moreover, NCX899 (but not enalapril) was effective in protecting against the cardiovascular changes induced by acute NOS inhibition.

SiRNA-mediated silencing of the diencephalic thyrotropin-releasing hormone precursor gene decreases the arterial blood pressure in the obese agouti mice

Obesity is associated with increased cardiovascular morbidity and mortality, in part through development of hypertension. Leptin promotes weight loss by reducing food intake and increasing energy expenditure through sympathetic stimulation. It also counteracts the starvation-induced suppression of thyroid hormone by up-regulating the expression of TRH. On the other hand, it is known that the extrahypothalamic TRH system participates in cardiovascular function modulating sympathetic system activity. In order to challenge the testable hypothesis that obesity may raise arterial blood pressure (ABP) through TRH system activation, we herein analyze the participation of the TRH system in the elevation of ABP in the obese agouti yellow mice. These mice are characterized by resistance to the weight reducing effect of leptin although they show a preserved sympathetic response to leptin along with a mild hypertension compared with the control strain (121+/-2 vs 102+/-2 mmHg, p less than 0.001, n=10). We report here that hyperleptinemic agouti mice showed a 1.8-fold elevation of diencephalic TRH content compared with controls, and we demonstrate that a long lasting specific inhibition of TRH system by icv treatment with siRNA against preproTRH normalizes systolic ABP independently of the thyroid status. These results suggest that the interaction leptin-diencephalic TRH may be one of the mechanisms involved in the mild hypertension of the obese agouti mice.

DISRUPTION OF NATRIURETIC PEPTIDE RECEPTOR A GENE INCREASES ADRENAL ANGIOTENSIN II AND ALDOSTERONE LEVELS.

The disruption of guanylyl cyclase/natriuretic peptide receptor A (GC-A/NPRA) gene (Npr1) leads to elevated arterial blood pressure, cardiac hypertrophy, congestive heart failure, and sudden death in mice lacking NPRA. ANP-NPRA signaling is known to counteract the renin-angiotensin-aldosterone system (RAAS). We studied whether Npr1 gene copy number affects adrenal angiotensin II (Ang II) and aldosterone (ALDO) levels in a gene-dose dependent manner in Npr1 gene-targeted mice. Adrenal Ang II and ALDO levels increased in one-copy (gene-disrupted heterozygous allele, 15%, p

Blood Pressure Response to Exercise Test and Serum Lipids in Normotensive Men with Positive Family History of Hypertension

The aim of the study was to follow the arterial blood pressure response to exercise test and serum lipids in middle-aged normotensive men with family history (FH) of arterial hypertension. 152 normotensive men, divided into two groups: I group--92 men without FH for arterial hypertension and II group--60 men with family history for arterial hypertension were investigated. The response of blood pressure to exercise test on bicycle ergometer with progressively increasing workload up to 100 W was followed up. Five minute recovery period was followed, too. The total cholesterol (TC), high-density and low-density lipoprotein cholesterol (HDL-C and LDL-C) and triglycerides were assessed and TC/HDL-C ratio was calculated. Significant difference in the arterial blood pressure at a level of 100 W between the Ist and IInd group was found: 177 +/- 19.0/ 89 +/- 12.0 mmHg versus 189 +/- 17**/ 96 +/- 11* mmHg (* p < 0.01, ** p < 0.001). Subjects with positive FH for arterial hypertension showed higher elevation of arterial blood pressure during and after exercise: OR = 2.3 (95% CI 1.1 -4.8). The systolic blood pressure during the recovery period and TC/HDL-C ratio were significantly higher with the Ilnd group. In conclusion, our data show significantly higher reaction of blood pressure to exercise, retarded recovery of blood pressure and significantly higher TC/HDL-C ratio with the individuals with positive FH for arterial hypertension.

Veno-Constriction of the Basilic Vein with Systemic Sympathetic Activation in Humans

Cardiac function is determined to a large extent by central venous volume-dependent cardiac filling pressure. Controlling the distribution of blood volume between the central and peripheral veins is therefore a key component of cardiovascular function. Reduction in peripheral venous volume via the muscle pump or vasoconstriction-induced passive venous recoil is well documented. However, in humans little is known about sympathetic venoconstriction, especially in larger conduit veins that drain the leg or arm. PURPOSE: To determine whether systemic sympathetic nervous system activation (SNA) can induce veno-constriction in human limb conduit veins. METHODS: 10 Male subjects lay supine with arms extended at heart level. Heart rate (HR) and mean arterial blood pressure (MAP) were measured using electrocardiogram (ECG) and arterial tonometry. Echo ultrasound was used to continuously measure basilic vein diameter ∼10–15 cm above the left elbow. Venous pressure was kept constant at 40 mmHg via inflation of a pressure cuff placed proximal to the site if vessel imaging. There were four experimental interventions: Physical Stress Evoked SNA (PS; maintained, vigorous lower limb isometric contraction), Mental Stress Evoked SNA (MS; STROOP word color test) Emotional Stress Evoked SNA (ES; anger interview), and a control condition (C; counting forward by one). Venous diameter was measured over 4 repeats of 2 minute baseline, 2 minute intervention, 4 minute recovery periods. The order of interventions was counter balanced. RESULTS: All data are mean VSE. All three SNA interventions resulted in significant reductions in venous diameter (mm) (baseline vs. intervention): PS – 5.91 ± 0.15 vs. 4.66 ± 0.26, P<0.05; MS – 5.85 ± 0.15 vs. 4.88 ± 0.16, P<0.05; ES – 5.90 ± 0.10 vs. 4.66 ± 0.32, P<0.05. No change was observed in the control intervention C – 5.91 ± 0.11 vs. 5.80 ± 0.12, P=NS. All three SNA interventions evoked significant increases in MAP (mmHg) (baseline vs. intervention): PS – 80.72 ± 1.81 vs. 112.50 ± 1.84, P<0.05; MS- 82.52 ± 1.86 vs. 96.12 ± 3.37, P<0.05; ES – 81.00 ± 2.49 vs. 91.71 ± 5.19, P<0.05. No change was observed in the control intervention C – 80.19 ± 2.39 vs. 83.11 ±2.90, P<0.05). CONCLUSION: Activation of systemic sympathetic nervous activity resulting in the elevation of arterial blood pressure is accompanied by constriction of the basilic conduit vein in humans. This confirms sympathetic innervation of this vein in humans and the capacity for human conduit vein volume to be regulated via sympathetic activation. Supported by: Natural Sciences and Engineering Research Council of Canada, Canada Foundation for Innovation, Ontario Innovation Trust

Orexin neuron-mediated skeletal muscle vasodilation and shift of baroreflex during defense response in mice

We have previously shown that some features of the defense response, such as increases in arterial blood pressure (AP), heart rate (HR), and ventilation were attenuated in prepro-orexin knockout (ORX-KO) mice. Here, we examined whether the same was true in orexin neuron-ablated [orexin/ataxin-3 transgenic mice (ORX/ATX-Tg)] mice. In addition, we examined other features of the defense response: skeletal muscular vasodilation and shift of baroreceptor reflex. In both anesthetized and conscious conditions, basal AP in ORX/ATX-Tg mice was significantly lower by approximately 20 mmHg than in wild-type (WT) controls, as was the case in ORX-KO mice. The difference in AP disappeared after treatment with an alpha-blocker but not with a beta-blocker, indicating lower sympathetic vasoconstrictor outflow. Stimulation of the perifornical area (PFA) in urethane-anesthetized ORX/ATX-Tg mice elicited smaller and shorter-lasting increases in AP, HR, and ventilation, and skeletal muscle vasodilation than in WT controls. In addition, air jet stress-induced elevations of AP and HR were attenuated in conscious ORX/ATX-Tg mice. After pretreatment with a beta-blocker, atenolol, stimulation of PFA suppressed phenylephrine (50 microg/kg iv)-induced bradycardia (DeltaHR=-360+/-29 beats/min without PFA stimulation vs. -166+/-26 during stimulation) in WT. This demonstrated the resetting of the baroreflex. In ORX/ATX-Tg mice, however, no significant suppression was observed (-355+/-16 without stimulation vs. -300+/-30 during stimulation). The present study provided further support for our hypothesis that orexin-containing neurons in PFA play a role as a master switch to activate multiple efferent pathways of the defense response and also operate as a regulator of basal AP.

Cardiac tamponade associated with an elevated arterial blood pressure

A 30-year-old male presented with acute pericarditis and a moderate pericardial effusion. His condition deteriorated suddenly with a marked elevation in blood pressure. The hypertension was erroneously correlated with a low probability of cardiac tamponade, leading to a delay in performing an echocardiogram. The echocardiogram subsequently showed features of cardiac tamponade. Severe elevation of blood pressure in a patient with cardiac tamponade is a rare and under-recognized disorder. This condition is discussed here.

Arterial Pressure Monitoring During Cardiopulmonary Bypass Using Axillary Arterial Cannulation

W g EMORAL ARTERIAL cannulation had been used as the alternate source of arterial inflow for cardiopulmonary ypass (CPB) when the ascending aorta or arch was unsuitable or various reasons. Right, or rarely left, axillary arterial canulations have become more common, especially when the emoral arteries are not available for arterial cannulation due to evere iliofemoral arterial disease1 or in patients who have evere atherosclerotic disease of the descending thoracic aorta ith floating debris that precludes safe retrograde arterial perusion.2 Right axillary artery cannulation may be the arterial nflow of choice in patients with aortic dissections and aortic neurysms3,4 when selective cerebral perfusion may be necesary during deep hypothermic circulatory arrest (DHCA).5 The uthors report a case in which monitoring of the ipsilateral adial arterial pressure in a patient on CPB using axillary annulation resulted in falsely elevated arterial blood pressures hat led to inappropriate hemodynamic management and hyoxic cerebral injury.

Alterations in Fetal Kidney Development and Elevations in Arterial Blood Pressure in Young Adult Sheep after Clinical Doses of Antenatal Glucocorticoids

Epidemiologic studies have yielded controversial information regarding an association between antenatal steroid administration and elevations in arterial blood pressure (BP). The aim of the study was to determine whether antenatal administration of a clinically relevant dose of steroids at a time when fetal nephrogenesis is at its highest results in abnormal kidney development and adult hypertension. Pregnant sheep were treated with either vehicle or betamethasone. Maternal injections were given 24 h apart at 80 d of gestational age (dGA; 0.55 of gestation). Animals were studied either as fetuses or as immature adults. Fetuses were delivered by cesarean section at 135 dGA. Adults were studied at 6 mo of age. Betamethasone administration did not induce premature labor or intrauterine growth restriction. In the betamethasone-exposed group, we found at 135 dGA a 25.5% decrease in the number of glomeruli with no differences in fetal kidney weight. In adults, mean, systolic, and diastolic arterial BPs were significantly higher, whereas there were no significant differences in heart rate over the same study period. The major finding of this study is that a single course of antenatal steroids alters renal development and is associated with elevations in arterial BP in lambs at 6 mo of age. We conclude that antenatal glucocorticoid administration under the National Institutes of Health consensus guidelines may alter human fetal renal development.

Blood Pressure and Vessel Recanalization in the First Hours After Ischemic Stroke

Transient elevation of arterial blood pressure (BP) is frequent in acute ischemic stroke and may help to increase perfusion of tissue jeopardized by ischemia. If this is true, recanalization may eliminate the need for this BP elevation. We analyzed BP in 149 patients with acute ischemic stroke on admission to the hospital and 1 and 12 hours after intraarterial thrombolysis. BP values of patients with adequate recanalization were compared with BP values of patients with inadequate recanalization. Recanalization was determined on cerebral arteriography after thrombolysis using thrombolysis in myocardial infarction grades. Systolic, mean, and diastolic arterial BP decreased significantly from admission to 12 hours after thrombolysis in all patients (P<0.001). Before thrombolysis, patients with adequate and inadequate recanalization showed equal systolic (147.4 and 148.0 mm Hg), mean (102.1 and 104.1 mm Hg), and diastolic (79.5 and 82.1 mm Hg) BP values. Twelve hours after thrombolysis, patients with adequate recanalization had lower values than those with inadequate recanalization (systolic BP, 130 versus 139.9 mm Hg; mean BP, 86.8 versus 92.2 mm Hg; and diastolic, BP 65.2 versus 68.3 mm Hg). Two-way repeated ANOVA analysis showed a significant group x time interaction for systolic BP, indicating a larger systolic BP decrease when recanalization succeeded (P=0.019). The course of elevated systolic but not diastolic BP after acute ischemic stroke was found to be inversely associated with the degree of vessel recanalization. When recanalization failed, systolic BP remained elevated longer than when it succeeded.

How low can you go? Intracranial pressure, cerebral perfusion pressure, and respiratory obstruction in children with complex craniosynostosis

Elevated intracranial pressure (ICP) is a well-recognized complication affecting children suffering from complex forms of craniosynostosis. The effects of ICP, including those on vision, and the underlying mechanisms involved remain uncertain. The aim of this study was to examine the relationships among ICP, cerebral perfusion pressure (CPP), and the episodic alterations in respiratory obstruction that are common in children with craniosynostosis. Eleven children with complex craniosynostosis underwent monitoring overnight, including simultaneous recording of subdural ICP, arterial blood pressure (ABP), and a variety of respiratory parameters. Sleep status was also analyzed. Mean values were calculated for all variables, including ICP, CPP, and ABP, during both quiet and active sleep. Mean ICP during quiet sleep was elevated in five patients, borderline in three, and normal in three children. During active sleep, plateaus of high mean ICP were observed in all patients. Marked decreases in CPP were demonstrated during active sleep with absolute values as low as 14 mm Hg. During quiet sleep, the mean baseline CPP was 53.3 mm Hg (range 34-70 mm Hg). During active sleep, CPP fell to a mean of 32.6 mm Hg (range 23-52 mm Hg). All patients experienced obstructive breathing problems, including 10 with obstructive sleep apnea, the effects of which demonstrated a temporal relationship to the alterations in sleep status, ICP, and CPP. Elevations of ABP appeared modest and remained within the normal limits for age. The findings of this study indicate that ICP, CPP, and respiratory obstruction interact in a vicious cycle, an observation that helps explain the pattern of plateau waves of elevated ICP characteristic among children with complex forms of craniosynostosis. The data gathered in this series revealed levels of CPP considerably lower than those described previously in clinical reports. Such reductions in CPP most likely contribute to the neurological, cognitive, and ophthalmological morbidity from which these children suffer frequently; therefore, the results of this study have important implications for the management of children with complex forms of craniosynostosis as well as for our understanding of the control of cerebral blood flow in general.

Parathyroid Hormone-Related Protein Overexpression Decreases Blood Pressure in Spontaneously Hypertensive Rats

We have recently demonstrated that arterial PTHrP expression and cardiovascular responses to this protein are altered in SHR compared with normotensive animals, Wistar Kyoto (WKY) and Sprague-Dawley (SD) rats. To investigate whether the slightly, but significantly decreased, aortic PTHrP gene expression observed in SHR, compared to that of normotensive animals, may play a causative role in the maintenance of the elevated arterial blood pressure (ABP) of the SHR, we transfected a hepatic lobe with a PTHrP expression vector in a sense and antisense orientation. At 24 and 48 hours, sense pSV2neo-ECE induced a significant five-fold increase in PTHrP mRNA abundance with respect to antisense pSV2neo-ECE and vehicle. This increment in the PTHrP mRNA induced by the sense PTHrP expression vector was totally inhibited by the co-administration of the antisense PTHrP expression vector. At the same time, we observed a significant decrease of mean ABP (MABP) in SHR transfected with the sense pSV2neo-ECE to similar values as those obtained in the normotensive strain. Neither antisense PTHrP expression vector nor vehicle had any significant effect in any strain. Again, the effect of the sense PTHrP expression vector on MABP was blocked by the simultaneous treatment with the antisense PTHrP expression vector. At 48 hours, the hypotensive effect of the sense pSV2neo-ECE in SHR was reverted by the IV bolus injection of a specific competitive PTHrP receptor antagonist such as Nle8,18,Tyr34-bPTH(3–34)amide. We propose that a defect of this potent local vasodilator may contribute to the development and/or maintenance of arterial hypertension in SHR. This defect can be ameliorated by transfecting tissues with protein-exporting capabilities, such as the liver. Finally, our work adds additional data to a cumulative body of evidence suggesting that it might be possible to design an effective gene therapy to treat the common polygenic and multifactorial form of hypertension by increasing the activity of potent and physiological vasodilators.

Effect of maturational status and training on upper limb pulse wave velocity

Cardiovascular adaptations to training may include changes in arterial distensibility, although studies involving sick and healthy individuals have yielded contradictory results. Moreover, despite the fact that endurance training frequently begins in childhood, its influence on arterial distensibility is less well characterised in children. This study was therefore to compare the upper limb pulse wave velocity (PWVUL) in highly trained prepubertal swimmers and age-matched moderately active counterparts, with that in swimmers and sedentary adults. The aim was to investigate the effects of maturation and training status on PWVUL in healthy individuals. PWVUL was evaluated by a dedicated continuous wave Doppler and photoplethysmography system. We calculated the pressure-corrected index of distensibility (Cp) which provides a measure of intrinsic structural compliance of the artery wall. PWVUL was significantly higher in highly trained child swimmers compared to moderately active ones (6.17+/-0.49 versus 5.20+/-0.38 ms(-1), P <0.05) even when mean arterial pressure was fixed as a covariate. Cp was significantly lower in child swimmers than in moderately active ones (0.15+/-0.03 versus 0.18+/-0.04, P <0.05 respectively) whereas Cp was not significantly different in either adult group. The PWVUL and Cp values of child swimmers were similar to those of adults. Our results confirmed an increase in pulse wave velocity with maturation implying that compliance decreases with age. An unexpected result was that swimming training performed in children over a long period led to an increase in upper limb pulse wave velocity. This change, concerning the upper limbs which are strongly involved in swimming, may be related to enhanced smooth muscle content of the arterial wall, possibly due to intermittent elevations in arterial blood pressure during repetitive swimming exercise sessions. Whether adaptations to intensive swimming training are accompanied by alterations of the cardiovascular system in prepubertal children is an important question to be dealt with in further studies.

Cardiorespiratory responses of the facultative air-breathing fish jeju, Hoplerythrinus unitaeniatus (Teleostei, Erythrinidae), exposed to graded ambient hypoxia

The jeju, Hoplerythrinus unitaeniatus, is equipped with a modified part of the swim bladder that allows aerial respiration. On this background, we have evaluated its respiratory and cardiovascular responses to aquatic hypoxia. Its aquatic O 2 uptake ( V˙ O 2 ) was maintained constant down to a critical P O 2 ( P cO 2 ) of 40 mm Hg, below which V˙ O 2 declined linearly with further reductions of P iO 2 . Just below P cO 2 , the ventilatory tidal volume ( V T) increased significantly along with gill ventilation ( V˙ G), while respiratory frequency changed little. Consequently, water convection requirement ( V˙ G/ V˙ O 2 ) increased steeply. The same threshold applied to cardiovascular responses that included reflex bradycardia and elevated arterial blood pressure ( P a). Aerial respiration was initiated at water P O 2 of 44 mm Hg and breathing episodes and time at the surface increased linearly with more severe hypoxia. At the lowest water P O 2 (20 mm Hg), the time spent at the surface accounted for 50% of total time. This response has a character of a temporary emergency behavior that may allow the animal to escape hypoxia.

Birth Weight Is Inversely Correlated to Adult Systolic Blood Pressure and Pulse Pressure in Type 1 Diabetes

In the general population, there is an inverse relationship between birth weight and adult systolic blood pressure. Because blood pressure in diabetic patients at least in part seems to be regulated by different mechanisms than in nondiabetic subjects, it is not known whether a similar correlation exists in diabetic individuals. Therefore, we obtained data on birth weight from original birth certificates in 1543 type 1 diabetic patients. Blood pressure was measured auscultatorily on a single occasion. In the 1225 patients born at term (after 37 weeks of gestation), the age- and sex-adjusted regression coefficients between systolic blood pressure and birth weight was -1.90 mm Hg/kg (95% confidence interval [CI], -3.71 to -0.09). The finding remained unchanged after adjustment for body mass index, current smoking, duration of diabetes, social class, antihypertensive therapy, glomerular filtration rate, glycemic control, and elevated albuminuria. The regression coefficient between birth weight and pulse pressure was of a similar magnitude. The age-adjusted regression coefficient between systolic blood pressure and birth weight seemed stronger in females (-3.34 mm Hg/kg; 95% CI, -6.06 to -0.62) than in males (-0.42 mm Hg/kg; 95% CI, -2.80 to 1.95), although this difference was not statistically significant. As a new finding, we report an inverse relationship between weight at birth and systolic blood pressure and pulse pressure in adult type 1 diabetic patients. Given the deleterious effects of elevated arterial blood pressure in diabetes, the impact of intrauterine growth retardation on the development of end-organ damage needs to be clarified.

Hemodynamics associated with breathing through an inspiratory impedance threshold device in human volunteers

Increased negative intrathoracic pressure during spontaneous inspiration through an impedance threshold device (ITD) causes elevated arterial blood pressure in humans. This study was performed to determine whether the acute increase in blood pressure induced by breathing through an ITD is associated with increased stroke volume and cardiac output. Randomized, blinded, controlled trial. Laboratory. Ten women and ten men. We measured hemodynamic and respiratory responses during two separate ITD conditions: 1) breathing through a face mask with an ITD (impedance of 6 cm H2O [0.59 kPa]) and 2) breathing through the same face mask with a sham ITD (control). Stroke volume was measured by thoracic bioimpedance. Compared with the control condition, ITD produced higher stroke volume (124 +/- 3 vs. 137 +/- 3 mL; p = .013), heart rate (63 +/- 3 vs. 68 +/- 3 beats/min; p = .049), cardiac output (7.69 vs. 9.34 L/min; p = .001), and systolic blood pressure (115 +/- 2 to 122 +/- 2 mm Hg [15.33 +/- 0.3 to 16.26 +/- 0.3 kPa]; p = .005) without affecting expired minute ventilation (6.2 +/- 0.4 to 6.5 +/- 0.4 L/min; p = .609). Breathing with an ITD at relatively low impedance increases systolic blood pressure by increasing stroke volume and cardiac output. The ITD may provide short-term protection against cardiovascular collapse induced by orthostatic stress or hemorrhage.

Acute postoperative hypertension: A review of therapeutic options

The pathophysiology and treatment of acute postoperative hypertension (APH) are discussed. APH is a significant elevation in arterial blood pressure (BP) during the immediate postoperative period. The predominant underlying mechanism appears to be sympathetic activation. APH may lead to serious neurologic, cardiovascular, or surgical-site complications and often requires intervention and management. Postoperative hypertension lasts less than six hours in most patients. Reversible or treatable causes of hypertension, including pain, anxiety, hypothermia, and hypoxemia, should be considered and treated before the implementation of antihypertensive therapy. The ideal agent for treating APH is intravenously administered, is fast acting, and has a short duration of action, allowing the rapid and safe adjustment of therapy to achieve a targeted BP range. Sodium nitroprusside has long been considered the standard therapy and has many of the ideal characteristics. However, because of the need for invasive hemodynamic monitoring and concerns about toxicity in patients given sodium nitroprusside, several newer agents may be preferable in routine clinical practice. Labetalol, nicardipine, and nitroglycerin have been widely studied or used. Hydralazine, esmolol, fenoldopam, angiotensin-converting-enzyme inhibitors, and clonidine may also be useful treatment options. When treatment of APH is necessary, therapy should be individualized for the patient. No one agent is preferred, but effective options include sodium nitroprusside, nitroglycerin, labetalol, and nicardipine.

Carotid chemoreceptor reflexes following dietary salt loading in rats

There is a strong association between salt intake and hypertension. Alterations in baroreceptor activity, which precede and contribute to the elevation in blood pressure, have also been shown to affect chemoreceptor reflex response. Dietary salt loading with 8% sodium chloride was carried out in Sprague Dawley rats aged 8 weeks for a period of 5-6 weeks. Blood pressure was thereafter recorded under anaesthesia from the common carotid artery with a Grass Polygraph 7D model, whereas serum Na[Formula: See Text] and K[Formula: See Text] concentrations were measured using a flame photometer. Salt loading resulted in elevated arterial blood pressure as well as hypokalaemia. Stimulation of the carotid chemoreceptor by injection of sodium dithionite resulted in elevated arterial blood pressure, decreased heart rate and hyperventilation in both control and salt-loaded rats. However, the bradycardic response as estimated by the difference in percentage reduction in heart rate was significantly higher in salt rats (36%) than in the control rats (10%). The results indicate that a high-salt diet results in enhanced bradycardic response to carotid chemoreceptor stimulation and that this observation may be related to the attendant hypokalaemia.