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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It was demonstrated earlier that the renal venous effluent of one-kidney, one clip hypertensive rats contained a vasodepressor lipid resembling the antihypertensive neutral renomedullary lipid (ANRL), following unclipping and as the arterial pressure (MAP) was lowered. Consequently, the sham-unclipped (clip-intact) and the unclipped kidney (CK and UCK) were studied by electronmicroscopy and morphometrically (Weibel's techniques). Renomedullary interstitial cells (RIC) of the CK had abundant granules. The collecting duct (CD) had tall lining cells containing pale granules and displayed intercellular channels. Following unclipping, the RIC degranulated and the CD cells became flattened, lost their pale granules, and the intercellular channels disappeared as the MAP decreased. These changes were evident by EM appearance and volume density measurements. The renopapillary changes occurred as the kidney secreted the ANRL-like substance into the blood.
Hypertension
PMID:Degranulation of renomedullary interstitial cells during reversal of hypertension. 729 42

Peritubular capillary hydrostatic and oncotic forces and their relationship to the renal excretion of sodium (UNaV) were examined in 19 patients with moderate and uncomplicated essential hypertension (HT) and compared with data from 20 normotensive subjects (NT). Observations were made in hydropenia (C) and during sustained isotonic saline volume expansion (E; 3% increase in body weight). The intrarenal venous pressure (IRVP) was used as an index of peritubular capillary hydrostatic pressure, and the efferent arteriolar colloid osmotic pressure (COPeff) was estimated from the arterial COP and the filtration fraction. C values (mean +/- SEM) in HT (and NT) were: arterial pressure (MAP) 110 +/- 3 mm Hg (85 +/- 1, p less than 0.001); glomerular filtration rate (GFR) 122 +/- 4 ml/min/1.73 m2 (128 +/- 3, p greater than 0.05); renal blood flow (RBF) 1172 +/- 38 ml/min/1.73 m2 (1298 +/- 48, p less than 0.05); IRVP 25.0 +/- 1.0 mm Hg (24.8 +/- 0.8, p greater than 0.05); COPeff 33.0 +/- 0.7 mm Hg (31.9 +/- 0.6, p greater than 0.05); and UNaV 140 +/- 13 mumole/min (161 +/- 12, p greater than 0.05). During E, the increase of UNaV in HT was more than double that of NT (p less than 0.001) while IRVP did not change in either group (p greater than 0.05); and COPeff fell by 26% (p less than 0.001) in both groups. GFR and RBF increased by 18% (p less than 0.001) and 19% (p less than 0.001) respectively, in HT, but did not change in NT. MAP remained unchanged in both groups. The results indicate that the peritubular capillary physical factors are normal in established essential hypertension, and that these forces are not involved in the exaggerated natriuretic response to volume expansion in essential hypertension.
Hypertension
PMID:Renal sodium excretion and the peritubular capillary physical factors in essential hypertension. 746 93

Hypertensive emergencies are uncommon and physiologically diverse. Consequently, it is difficult for most physicians to develop a familiarity with all the different hypertensive crises and with all drugs available for treating them (Table 4). Clinicians should not agonize over which is the perfect therapeutic agent for a particular emergency, but instead, they should focus on scrupulous monitoring and familiarize themselves with a few agents that will serve in most situations. Generally, these agents will be sodium nitroprusside and nitroglycerin. Vigilant neurologic monitoring is mandatory in all hypertensive emergencies. The early symptoms and signs of cerebral hypoperfusion can be vague and subtle, but if recognized, serious complications of therapy can be avoided. Remember, the patient may still be hypertensive. Avoid acute (during the first hour) reductions in MAP of more than 20% whenever possible; subsequent reductions should be gradual. In patients known to have markedly elevated ICP and who need acute reductions in their BP, serious consideration should be given to direct monitoring of the ICP so that CPP can be maintained within safe limits. In general, oral agents should not be used for the treatment of hypertensive emergencies. Intravenous Labetalol and intravenous nicardipine are not suitable for general use in hypertensive emergencies. In special situations (e.g., perioperative hypertension and subarachnoid hemorrhage), however, they may be employed. Their role may expand with further study. Trimethaphan may be superior to nitroprusside for hypertension complicated by elevated ICP or cerebral dysfunction. Realistically, most physicians will continue to use nitroprusside. Intense neurologic monitoring is more important than the specific agent used. Nitroglycerin is the agent of choice for acute ischemic heart disease complicated by severe hypertension; if it fails, use nitroprusside. For aortic dissection, the combination of nitroprusside and IV propranolol is the therapy of choice; beta-blockade must be achieved rapidly or the dissection may worsen. Trimethaphan is also an agent for first-line therapy. Esmolol is an alternative to IV propranolol for the treatment of aortic dissection, if prolonged beta-blockade might seriously jeopardize the patient. For eclampsia, unless an expert in hypertension during pregnancy has established an alternative, the therapy of choice is hydralazine and magnesium. The treatment of subarachnoid hemorrhage is in flux; calcium channel blockers are used to prevent spasm, not to lower BP. If the BP must be lowered immediately, use nitroprusside.
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PMID:Hypertensive emergencies. 758 98

The effects of arterial pressure on cerebral reactive hyperaemia were studied in anaesthetized goats measuring electromagnetically middle cerebral artery flow and performing arterial occlusions of 5-30 s. Under normotension (mean arterial pressure, MAP = 11 +/- 0.3 kPa), reactive hyperaemia (peak hyperaemic flow to control flow and repayment to debt ratios) increased, and cerebrovascular resistance during peak hyperaemic flow decreased, as ischaemia duration lengthened; the virtual maximal changes were obtained after 20 s ischaemia. During hypertension by aorta constriction (MAP = 18 +/- 0.7 kPa) or by i.v. infusion of noradrenaline (MAP = 19 +/- 0.8 kPa) middle cerebral artery flow did not change significantly and cerebrovascular resistance increased 25 and 46%, respectively (P < 0.05). During both types of hypertension reactive hyperaemia was over 50% higher, and the decrement in cerebrovascular resistance during peak hyperaemic flow was also higher, than under normotension. During hypotension by constriction of the inferior vena cava (MAP = 5 +/- 0.5 kPa) or by i.v. infusion of isoproterenol (MAP = 6 +/- 0.5 kPa), middle cerebral artery flow decreased 35% or did not change, and cerebrovascular resistance decreased 41 and 45%, respectively (P < 0.05). In these conditions, reactive hyperaemia and the decrement in cerebrovascular resistance during peak hyperaemic flow were reduced 80%, and it was similar in both types of hypotension. The absolute levels of cerebrovascular resistance obtained during peak hyperaemia were similar during normotension, hypertension and hypotension. Thus, arterial pressure is a main determinant of postocclusive cerebral reactive hyperaemia, and myogenic mechanisms may be of significance in determining the early stage of cerebral reactive hyperaemia after brief ischaemias. Adrenergic mechanisms might be of minor significance in this type of cerebral reactive hyperaemia.
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PMID:Cerebral reactive hyperaemia and arterial pressure in anaesthetized goats. 761 82

Adenosine is a potent arterial vasodilator that, because of a short duration of action and acid lability, is ineffective in the oral treatment of hypertension. Y-341 is a synthetic adenosine analog that is acid stable and has a prolonged duration of action. It is highly selective for the A2 receptor, which is prevalent in the vascular smooth muscle and mediates vasodilation. To determine the efficacy of Y-341 as an antihypertensive agent, the effect of Y-341 on arterial pressure was studied in spontaneously hypertensive rats (SHR) in the awake state, 3 to 4 days after arterial cannulation. Y-341 (3 mg/kg) was dissolved in 5% DMSO and administered by gavage. Blood pressure and heart rate were monitored continuously at predetermined intervals. Fifteen minutes after administration, Y-341 reduced MAP from 180 +/- 4 to 126 +/- 2 mm Hg (n = 9, P < .001). There was no significant change in heart rate. The hypotensive effect was sustained over 8 h. Vehicle (n = 5) had no effect on blood pressure. The hypotensive effect was dose dependent when the dose of Y-341 was increased from 3 to 6 and 12 mg/kg. When Y-341 was administered at 3 mg/kg/day in a single dose for 5 consecutive days, there was no significant change in the magnitude of the hypotensive response over time.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The hypotensive effect of an oral adenosine analog with selectivity for the A2 receptor in the spontaneously hypertensive rat. 766 28

Ambulatory blood pressure was measured in 23 microalbuminuric Type 1 diabetic patients without hypertension. Nine patients had a reduction in mean arterial blood (MAP) pressure at night < 10% of their day-time value (non-dippers). The following parameters were measured: glomerular filtration rate (GFR), overnight urinary excretion of albumin (UAE), sodium and potassium, left ventricular dimensions, extracellular volume (ECV), plasma aldosterone, and arginine vasopressin (AVP). Night-time MAP was 11 mmHg lower in patients designated as dippers than in non-dippers. Day-time MAP was similar in dippers (98 +/- 5 mmHg) and non-dippers (99 +/- 8 mmHg, NS). No statistical significant difference was found for UAE in dippers (geometric mean, x/- tolerance factor, microgram min-1) (72 x/- 2.1) vs non-dippers (63 x/- 2.1), for left ventricular mass index (63 +/- 12 vs 59 +/- 10 g m-2), or for GFR (134 +/- 19 vs 148 +/- 22 ml min-1). Aldosterone and AVP were lower in non-dippers (p < 0.05) and a negative correlation in all patients was noticed between ECV and aldosterone (rho = -0.50, p < 0.05). Sodium and potassium excretion and ECV were indistinguishable between the groups. We conclude (1) that impaired reduction of night blood pressure does not seem to be associated with more signs of renal or cardiac lesions and (2) that the lower aldosterone and AVP in non-dippers may counteract volume expansion.
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PMID:Night blood pressure: relation to organ lesions in microalbuminuric type 1 diabetic patients. 771 2

To assess the effects of cocaine, administered to the ewe, on the secretion of atrial natriuretic peptide (ANP), Plasma Renin Activity (PRA) and hypoxanthine in the fetus we studied 6 chronically cannulated sheep fetuses late in gestation. The ewe was given an intravenous injection of cocaine (2 mg/kg). Maternal and fetal arterial blood samples were withdrawn prior to the injection and at 2, 5, 10, 15, 45 and 60 min after the injection for the measurement of ANP, PRA and hypoxanthine. Fetal arterial blood pressure (MAP), plasma ANP and protein levels increased and pH and pO2 decreased after cocaine was administered to the ewe. Fetal plasma hypoxanthine and PRA did not change. These results suggest that cocaine administration to the ewe is associated with fetal hypertension, hypoxemia and acidemia all of which may serve as stimuli for the secretion of ANP.
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PMID:Intrauterine exposure to cocaine increased plasma ANP (atrial natriuretic peptide) but did not alter hypoxanthine concentrations in the sheep fetus. 772 97

Circulating angiotensin II (ANG II) has several physiological effects that result from interaction of the peptide with AT1 receptors in the brain. Our purpose was to determine if selective pharmacological blockade of brain AT1 receptors would reverse chronic low-dose ANG II-induced hypertension. Male Sprague-Dawley rats were instrumented with chronic indwelling arterial and venous catheters and a lateral intracerebroventricular (i.c.v.) cannula. All rats received ANG II i.v. for 15 days at a dose of 4 ng.min-1. On days 2, 7 and 12 of the ANG II infusion a bolus of an AT1 receptor antagonist, the active metabolite of losartan, EXP 3174 (1 microgram in 2 microliters of saline, i.c.v.; n = 5) or vehicle (2 microliters of saline; n = 2) was administered into the cerebrospinal fluid. Mean arterial pressure and heart rate were measured at numerous time points after this injection. Although the dose of EXP 3174 used in preliminary experiments was shown to block the responses to i.c.v. ANG II this treatment did not lower MAP in chronic ANG II-hypertension. These results suggested that either ANG II-hypertension does not involve brain AT1 receptors, or that i.c.v. EXP 3174 may not gain access to brain sites at which circulating ANG II acts to produce hypertension. To test this latter possibility ANG II was microinjected into the area postrema of anesthetized rats. The area postrema is one of several circumventricular organs at which circulating ANG II may act to influence arterial pressure regulation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cerebroventricular injection of angiotensin II antagonist: effects on blood pressure responses to central and systemic angiotensin II. 775 62

ACE-inhibitors are known to have special renal effects, i.e. they increase ERPF, decrease the filtration fraction and lower proteinuria. These effects can be due to a decrease in angiotensin II (AII) levels as well as an increase in bradykinin. New and more specific AII-receptor antagonists may help to distinguish between effects exerted by angiotensin II and those exerted by bradykinin. We investigated the effects of losartan in 9 patients with essential hypertension (sitting mean diastolic blood pressure 95-120 mmHg). Renal hemodynamics were measured by continuous inulin-and PAH-clearance (GFR and RPF) after stopping antihypertensive therapy for 1 week, followed by a 2-week placebo period and after a 4-week treatment phase with losartan (50 mg/die) followed by a therapy with an ACE-inhibitor (ramipril 5mg/die). Additionally, urine albumin excretion (UAE) was measured. Treatment of patients with essential hypertension with losartan resulted in a significant decrease of MAP after three weeks of treatment (121 +/- 8 mmHg under placebo and 114 +/- 10 mmHg under losartan; * = p < 0.05). MAP after four weeks of losartan treatment was 115 +/- 11 mmHg. Regarding changes in renal hemodynamics we could not demonstrate a significant change for neither losartan nor the ACE-inhibitor. Urine albumin excretion was reduced by both treatment regimens in correlation to the magnitude of blood pressure reduction. Our data indicate that losartan induced a significant reduction in MAP in patients with essential arterial hypertension with only moderate effects on renal hemodynamics.
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PMID:Renal hemodynamics in essential hypertensives treated with losartan. 778 Dec 6

While the importance of receptor-mediated intracellular cyclic AMP in blood pressure regulation is well documented, few studies have evaluated the physiologic relevance of cyclic AMP exported from cells. We report evidence of a relationship between blood pressure and the transport of intracellular cyclic AMP from lymphocytes. Twenty-eight hypertensive and 56 normotensive white and black volunteers (mean age 40 years) were studied. Both intra- and extracellular concentrations of cyclic AMP were determined in lymphocytes following incubation with 10(-5) M isoproterenol. Compared to normotensives, hypertensives (p = 0.001), particularly white hypertensives (p = 0.023) had higher levels of exported cyclic AMP. These values were independent of intracellular concentrations of cyclic AMP, which were similar across the groups. Exported cyclic AMP was independent of both sodium excretion and beta-adrenergic receptor sensitivity, the latter being lower in white hypertensives (p = 0.024). Across all subjects, exported cyclic AMP was correlated with MAP (r = .39, p < 0.001). These findings indicate that the active transport of cyclic AMP may be enhanced in hypertension and suggest a possible pathway which might explain existing data of increased cyclic AMP levels in hypertension.
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PMID:Cyclic AMP export from lymphocytes in hypertension. 785 62


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