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

The role of central nervous system (CNS) catecholamines in the development of hypertension and the control of drinking behavior was assessed in rats by depleting these amines with 6-hydroxydopamine (6-OHDA). Intraventricular administration of 6-OHDA completely prevented the development of one-kidney renal hypertension and abolished the associated increase in water consumption. 6-OHDA-treated rats showed deficits in drinking behavior when challenged with subcutaneous injections of angiotensin II (AII) and hypertonic sodium chloride. The acute pressor responses produced by intraventricular injections of AII and carbachol were virtually abolished by central catecholamine depletion. However, drinking produced by central cholinergic stimulation remained intact while AII drinking was significantly reduced. These data demonstrate that the integrity of CNS catecholamines is required for the development of one-kidney renal hypertension and the increased drinking which accompanies it. In addition, destruction of central catecholamine-containing neurons allows for a specific dissociation of the pressor and drinking responses produced by central cholinergic but not AII stimulation.
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PMID:Role of central catecholamines in the control of blood pressure and drinking behavior. 49 58

Adrenal responsiveness to angiotensin II (AII) and the diastolic blood pressure responses to saralasin were studied in 19 patients with high renin essential hypertension (HREH) on a 10-meq Na(+)/100 meq K(+) diet. The increment in plasma renin activity (PRA) between supine and upright positions was used as an estimate of the acute stimulation of the adrenal gland by endogenous AII; the normal increment in plasma aldosterone divided by the increment in PRA was >3.8. 7 of 19 had abnormal upright posture responses with significantly greater mean PRA increments (24+/-6 ng/ml per h) and significantly smaller plasma aldosterone increments 47 +/- 16 ng/dl) (P < 0.036) compared to the increments observed in HREH patients with normal adrenal responsiveness (PRA = 15 +/- 1 ng/ml per h; plasma aldosterone = 87 +/- 17 ng/dl). When AII was infused at doses of 0.1-3 ng/kg per min, only patients with normal posture responses had normal plasma aldosterone increments; plasma aldosterone levels failed to significantly increase even at the highest infusion rate in the patients with the abnormal upright posture responses. The AII competitive inhibitor, saralasin (0.3-30 mug/kg per min) was then infused to study the occurrence of angiotensinogenic hypertension in both HREH subgroups. The mean decline in diastolic blood pressure to saralasin in the subnormal adrenal responsive patients (-15 +/- 3 mm Hg) was significantly greater than in the normal adrenal responsive group (-3 +/- 2 mm Hg) (P < 0.02).It is concluded that patients with HREH are not a homogeneous population; approximately one-third have AII-dependent hypertension. In these patients, the mechanism responsible for the elevated renin and blood pressure could be a compensatory increase secondary to decreased adrenal responsiveness to AII. In the remainder, the high PRA levels have little, if any, causal role in the pathogenesis of the hypertension but could reflect a marker of other pathophysiologic processes.
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PMID:Abnormal adrenal responsiveness and angiotensin II dependency in high renin essential hypertension. 50 Aug 10

Plasma catecholamine levels have been used experiemtally and clinically as the indices of the sympathetic nerve activity. We measured plasma catecholamines using high pressure liquid chromatography in rats to assess the significance of plasma catecholamines as an index of the sympathetic nerve activity and its role in hypertension. Pentobarbital anesthesia depressed plasma catecholamine levels, especially plasma adrenaline. Sodium loading for 5 weeks suppressed plasma noradrenaline, while administration of furosemide (1 mg/kg) produced the elevation of plasma noradrenaline. Experimental hypertension, one-kidney and two-kidney types of Goldblatt hypertension and DOCA-salt hypertension, raised plasma noradrenalines both in acute and chronic phases. The infusion of pressor doses of angiotensin II suppressed plasma noradrenaline by the reflex mechanism. Sar1, Ile8-angiotensin II and SQ 14,225 did not suppress plasma cathecholamine elevation due to hemorrhage. L-Hydroxyldopamine produced elevation of plasma catecholamines in experimental nypertension and controls in rats. After adrenal demedullation, plasma noradrenaline was decreased by the administration of 6-hydroxy-dopamine. Acute reduction of circulating blood volume and blood pressure fall produced the elevation of plasma catecholamine, especially plasma adrenaline. In rats, the adrenal medulla plays an important role in the regulation of blood pressure.
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PMID:Plasma catecholamines determination using high pressure liquid chromatography and their roles in blood pressure regulation and experimental hypertension in rats. 50 4

The rare opportunity arose to assess in detail the renin-angiotensin system before and after the development of a renal artery stenosis with severe hypertension. Peripheral plasma concentrations of renin, angiotensin II, and aldosterone were known to be normal before the development of renal artery stenosis, and there were no lateralising features on renal vein sampling. Acute hypertension associated with very high peripheral plasma concentrations of renin and angiotensin II, and with pronounced lateralisation on renal vein sampling followed the development of acute unilateral renal artery stenosis. These measurements all returned to normal after nephrectomy, conforming with the pattern of changes previously established only in experimental animals.
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PMID:Renal artery stenosis with severe hypertension. A rare case with detailed assessment of renin-angiotensin system before and after development of lesion. 50 79

1. To characterize the renin-angiotensin-aldosterone system in elderly hypertensive patients, an angiotensin II antagonist, [Sar1,Ile8]angiotensin II, was infused into individuals 60 years old and older with and without hypertension. 2. After infusion of [Sar1,Ile8]angiotensin II in all of the elderly patients and subjects an agonistic pressor response was observed that was greater than in middle-aged hypertensive patients. 3. Pre-infusion plasma renin activity and plasma aldosterone concentration in hypertensive and normotensive elderly groups were suppressed in comparison with those in middle-aged hypertensive subjects. The increased agonistic effects of [Sar1,Ile8]angiotensin II infusion on blood pressure in the elderly are presumably due to their hyporeninaemia. 4. The angiotensin-aldosterone system in elderly essential hypertensive patients is suppressed and is presumably not responsible for their elevated blood pressures.
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PMID:Studies on the renin-angiotensin-aldosterone system in elderly hypertensive patients with an angiotensin II antagonist. 51 55

The purpose of the present work was to measure prostaglandin (PG)-like activity in arterial blood during acute pulmonary hypertension. Anesthetized cats with the chest opened and given positive pressure ventilation were used. A balloon in the left atrium was inflated to elevate hydrostatic vascular pressure in the lungs. Blood was pumped (10 ml/min) from a carotid artery to superfuse 3 smooth muscle tissues: rat stomach strip, rat colon and chick rectum: the blood was then returned to the jugular vein by gravity. The assay tissues were pretreated with antagonists against catecholamines, histamine, serotonin and acetylcholine during the experiments. They were sensitive to calibrating doses of 2 ng/ml of PGF2 alpha and 1 ng/ml of PGE2. 18 periods with elevated left atrial pressure (P LA) (21--49 mmHg), lasting 2--26 min, were applied in 9 cats. This manoevre usually also caused systemic hypotension. 14 of these PLA elevations were accompanied by increased arterial PG-like activity, which rapidly subsided when the pressure was released or when indomethacin (2 mg/kg, n = 4) was given i.v. In 3 additional experiments it was found that pulmonary degradation of PGs was unaffected during P LA elevation. I.v. infusion of angiotensin II contracted the tissues in a pattern different from that caused by pressure elevations and the PG calibrations, and these contractions were not affected by indomethacin. This indicates that the assay tissue contractions cannot be caused by angiotensin II which alone does not increase PG-like activity in arterial blood. Consequently, acute pulmonary vascular hypertension appears to stimulate PG synthesis and release in lungs of intact cats.
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PMID:Release of prostaglandin-like substances during elevations of left atrial pressure in the cat. 52 82

Saralasin (S) infusion, at a dose of 10 micrograms/kg/min IV, decreased Glomerular Filtration Rate (GFR) in 18 hypertensive patients. This effect was more pronounced in those patients with angiotensinogenic hypertension due to the somation of the effects of S upon renal vasculature and systemic arterial pressure. A decrease in urinary sodium excretion was also observed being more intense in those patients whose systemic pressure also decreased during S infusion. In group II (10 hypertensive patients) infusion of S in increasing doses (0.1, 0.5, 1.0, 5.0 and 10.0 micrograms/kg/min) a progressive decrease in GFR was observed only when the arterial pressure also decreased. However urinary sodium excretion decreased progressively as S doses increased. This effect was not related to S effect upon arterial pressure. This observation indicates that S, like angiotensin II, has a direct effect upon the renal tubules evoking an increase of sodium reabsorption.
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PMID:[Effect of saralasin infusion on glomerular filtration rate and sodium excretion in hypertensive patients (author's transl)]. 53 Dec 73

1. Alterations in vascular reactivity were assessed in isolated artificially perfused kidneys from stroke-prone spontaneously hypertensive (spSH) rats at different stages of hypertension and after neonatal sympathectomy with 6-hydroxydopamine (6-OHDA). 2. During the pre-hypertensive stage, and the early and chronic stages of hypertension, the responses to noradrenaline, vasopressin, serotonin and angiotensin II were enhanced in renal vascular beds from spSH animals compared with age- and sex-matched Wistar-Kyoto (WK) rats; dose-response curves were shifted to the left, had steeper slopes, greater maximal responses and decreased thresholds. 3. With increasing severity and duration of hypertension, renal vascular resistance at maximal vasodilatation increased, the slopes of the dose-response curves were steeper and maximal responses were greater. 4. Neonatal sympathectomy with 6-OHDA greatly attenuated but did not prevent the eventual development of hypertension; furthermore, this treatment had no effect on the enhanced resistance or reactivity in renal vascular beds from spSH rats. 5. The appearance of enhanced resistance and reactivity in the early stages of hypertension and the inability to prevent these vascular changes by neonatal sympathectomy suggest that these alterations are a primary pathogenic mechanism in spSH rats.
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PMID:Vascular reactivity in the pathogenesis of spontaneous hypertension. 54 Apr 70

Guancydine (1-cyano-3-tert-amylguanidine) lowered within normal limits the tensional values in an interval of four hours after its administration in eight out of nine hypertensive patients under experiment. The hypotensive effect of a single oral dose of 500-750 mg persists for about 6-7 hours after its administration. Guancydine does not impair the vasopressor response to angiotensin II but reduces the action of this peptide on the excretion of water, Na, K and Ca through urine. The hypotensive effect of Guancydine is associated with a decrease of platelet adhesiveness and an activation of fibrinolysis. In view of this fact, Guancydine might play a role in the prophylaxis of complications of arterial hypertension - atherosclerosis and trombosis. The increase of venous blood oxygenation after Guancydine could be attributed to the opening of arterio-venous shunts or to the reduction of tissular extraction of oxygen. Guancydine does not seem to be toxic. It produced, in some patients, slight headache and orthostatic hypotension, especially during the first hours after administration.
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PMID:Guancydine, a new hypotensive agent with complex action. 56 30

A patient with intractable congestive cardiac failure secondary to renovascular hypertension and severe coronary artery disease was infused with the competitive antagonist of angiotensin II, saralasin acetate. The infusion produced an impressive increase in cardiac output and left ventricular stroke work index in parallel with a striking decrease in the systemic and pulmonary vascular resistance, the coronary resistance, and the myocardial oxygen consumption. It is suggested that angiotensin inhibition may present advantages over other forms of treatment of congestive cardiac failure in selected cases.
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PMID:Angiotensin II inhibition. Treatment of congestive cardiac failure in a high-renin hypertension. 57 78


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