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

Cardiovascular hypertrophy plays an important role in the development and maintenance of hypertension. Hyperactivity of the sympathetic nervous system may be one of the initiating factors responsible for the stimulation of growth processes involved in these structural alterations. We have used a well-established early biochemical marker of cellular growth processes, induction of ornithine decarboxylase (ODC), to determine whether alpha 1-adrenergic receptor-induced vascular trophic responses are dependent on arterial pressure elevation. Hydralazine or felodipine were coadministered to control the alpha 1-adrenergic receptor agonist-induced rise in mean arterial pressure (MAP). Methoxamine (2, 5, or 10 mg/kg s.c.) increased the average MAP (up to 20 mm Hg) and vascular ODC activity (up to ninefold) above control rats over 4 hours. Concomitant administration of hydralazine (0.5, 1.25, or 5 mg/kg s.c.) or felodipine (100 or 250 micrograms/kg s.c.) with methoxamine (10 mg/kg) attenuated the alpha 1-adrenergic receptor-induced activation of ODC in the aorta and mesenteric resistance vasculature, as well as the MAP increases. Vasodilators alone did not lower basal vascular ODC activity. The major findings include: 1) alpha 1-adrenergic receptor activation dose-dependently induces vascular ODC activity concomitantly with MAP elevation, 2) vasodilators inhibited both the alpha 1-adrenergic receptor-induced MAP increases and the activation of mesenteric vascular and aortic ODC, and 3) the stimulus-response correlation between MAP elevation and mesenteric (r = 0.78) and aortic (r = 0.92) ODC activation was characterized by a logistic function.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1992 Dec
PMID:Vasodilators inhibit acute alpha 1-adrenergic receptor-induced trophic responses in the vasculature. 136 Apr 48

Cocaine abuse is widespread, and its use by the parturient has potential significant adverse effects in both the mother and the newborn. This study was undertaken in gravid ewes to determine the effects of treatment of cocaine-induced hypertension with hydralazine (Apresoline) on the maternal and fetal cardiovascular systems, catecholamine response, blood gas and acid-base status, and uterine blood flow (UBF). Twenty-one experiments were performed in 15 chronically instrumented ewes near term gestation. After a 30-min control period, cocaine was given intravenously to all ewes for 55 min to induce and maintain increased maternal mean arterial pressure (MMAP) and reduced UBF. The sheep were randomly assigned to receive either cocaine alone (n = 11, control group) or hydralazine (n = 10, treatment group), starting 15 min after the cocaine administration. Both drugs were discontinued 55 min after the start of the cocaine administration, followed by a 35-min recovery period. In the control group, cocaine administration resulted in a 31 +/- 13% (SD) increase in MMAP (P less than 0.05) and a 26 +/- 21% reduction in UBF (P less than 0.05). In the treatment group, the initial cocaine administration resulted in a similar increase in MMAP and decrease in UBF. Hydralazine therapy restored MMAP toward baseline after 20 min of administration, but UBF remained reduced (37 +/- 17%) throughout therapy (P less than 0.05) and recovery (18 +/- 13%) (P less than 0.05). The maternal heart rate increased maximally by 121 +/- 33% (P less than 0.05) after the administration of hydralazine, compared with a 14 +/- 21% increase (P less than 0.05) in the control group.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hydralazine does not restore uterine blood flow during cocaine-induced hypertension in the pregnant ewe. 155 Feb 83

In this study, the effect of the antihypertensive agents nifedipine (4.5 mg/day) and hydralazine (50-200 mg/l of drinking water) on the progression of chronic renal failure and scarring was evaluated in rats submitted to subtotal (5/6) nephrectomy (SNx). The effect of blood pressure reduction was studied in groups of rats fed either a medium-protein diet (24%) or high-protein diet (50%). SNx rats fed a high-protein diet had significantly higher levels of proteinuria and severer renal scarring at sacrifice (120 days after SNx). Nifedipine reduced proteinuria in SNx rats fed a high-protein diet. Both drugs significantly reduced systemic hypertension in SNx rats. Hydralazine and nifedipine also reduced hypertriglyceridaemia but had no effect on blood cholesterol levels. However, in spite of adequate control of systemic hypertension with the agents studied, the severity of renal scarring (glomerular sclerosis or tubulo-interstitial scarring) was not affected by treatment. We confirm that the control of systemic hypertension is not sufficient to prevent renal scarring in rats submitted to extensive renal ablation.
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PMID:Effect of antihypertensive therapy in experimental chronic renal failure. 182 85

The goal of the present study was to compare the effects of cilazapril, a new long-acting angiotensin converting enzyme inhibitor, to those of captopril and hydralazine on the coronary vascular bed. For this purpose, spontaneously hypertensive rats were treated for 4 months with either placebo, 10 mg/kg/day cilazapril, 100 mg/kg/day captopril, or 10 mg/kg/day hydralazine. At the end of treatment, maximal coronary blood flow was measured during maximal coronary vasodilation with adenosine in isolated perfused hearts. Cilazapril was the most effective drug in increasing maximal coronary blood flow. Captopril was less effective in improving maximal coronary blood flow but was as effective as cilazapril in reducing cardiac hypertrophy. Hydralazine had an extremely small effect on cardiac hypertrophy and maximal coronary flow reserve. The ranking of efficacy was similar for the reduction of vessel wall hypertrophy in the coronary arteries and arterioles. Because of the higher efficacy of cilazapril compared with captopril, a second experiment was performed in which 10 mg/kg/day cilazapril was compared with 100 mg/kg/day captopril and 300 mg/kg/day captopril after 1 month of treatment. Captopril increased maximal coronary flow and decreased cardiac hypertrophy to the same level as cilazapril only at the highest dose. We conclude that angiotensin converting enzyme inhibitors, in contrast to hydralazine, can increase markedly maximal coronary flow in spontaneously hypertensive rats but that this increase does not always parallel the decrease of cardiac hypertrophy and is closely dose dependent.
Hypertension 1991 Oct
PMID:Effects of two angiotensin converting enzyme inhibitors and hydralazine on coronary circulation in hypertensive rats. 183 28

This manuscript describes changes in the steady state levels of aortic tropoelastin mRNA in spontaneously hypertensive rats (SHR) and normotensive controls (WKY) following treatment with two antihypertensive drugs. Three-week-old WKY and SHR rats were treated with hydralazine (15 mg/kg/day) or captopril (25 mg/kg/day). Tail artery blood pressure was monitored twice weekly. Both drugs prevented the development of hypertension in the SHR rat. At 6 weeks of age, total aortic RNA was extracted and the steady state levels of mRNAs coding for tropoelastin and pro alpha 1 (III) collagen were determined by slot blot hybridization analysis using radiolabeled tropoelastin and pro alpha 1 (III) collagen cDNA clones. Hydralazine treatment resulted in a threefold increase in tropoelastin mRNA levels in both the SHR and the WKY animals (P less than 0.01). Captopril-treated SHR animals demonstrated a similar significant increase. In contrast, no differences in pro alpha 1 (III) collagen mRNA levels were observed in the aorta of SHR or WKY rats following treatment with either captopril or hydralazine. These data suggest that antihypertensive agents can act specifically to directly induce tropoelastin mRNA levels in large arteries and thus may induce vascular remodeling independent of an increase in blood pressure.
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PMID:Changes in aortic levels of tropoelastin mRNA following treatment of rats with the antihypertensive drugs captopril and hydralazine. 194 85

The effects of chronically administered hydralazine on adrenergic neurotransmission were evaluated in the perfused mesenteric artery of spontaneously hypertensive rats (SHR) preloaded with [3H]norepinephrine. The 3H overflow evoked by periarterial nerve stimulation (PNS, 2-32 Hz) was greater in both young (5-week-old) and adult (13-week-old) ages of SHR in comparison with age-matched Wistar Kyoto rats (WKY). Hydralazine treatment, which prevented the development of hypertension, attenuated the increased 3H overflow evoked by PNS in SHR. At adult age, the logarithmic value for the concentration (nM) of salbutamol to cause a 20% enhancement of the evoked 3H overflow was significantly smaller in SHR than in WKY. The increased sensitivity of presynaptic beta-adrenoceptors in SHR was reduced by hydralazine treatment. The concentration-response curve of the facilitation of the evoked 3H overflow caused by salbutamol in hydralazine-treated SHR lay between the curves in SHR and WKY. No significant difference in the inhibitory effects of xylazine on the PNS-evoked 3H overflow was found among SHR, hydralazine-treated SHR and WKY. At young age, presynaptic alpha- and beta-adrenoceptors were supersensitive in SHR. The results suggest that an altered adrenergic neurotransmission mediated by presynaptic beta-adrenoceptors in adult SHR is partially improved by chronic hydralazine administration, this accounting for the attenuation of the increased norepinephrine release observed in hydralazine-treated SHR.
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PMID:Effect of chronically administered hydralazine on altered adrenergic neurotransmission mediated by presynaptic alpha- and beta-adrenoceptors in spontaneously hypertensive rats. 196 98

In patients with hypertension persisting on combined diuretic and beta-blocker therapy, the effects of an additional 9-week therapy with a calcium antagonist (nifedipine) versus a classical arterial vasodilator (hydralazine) were compared for changes in blood pressure (BP), plasma catecholamines (n = 15), and left ventricular (LV) systolic and diastolic function (n = 6). Both drugs lowered BP, but nifedipine was significantly more effective in lowering systolic BP. Hydralazine increased both supine and standing plasma norepinephrine, nifedipine increased them only in the standing position and to a lesser extent. Patients on beta1-selective (n = 5) versus nonselective (n = 10) blockade showed similar responses. Left ventricular systolic function was not affected by hydralazine, whereas nifedipine increased the rate of ejection. In contrast, LV diastolic function was not affected by nifedipine, whereas hydralazine improved the peak filling rate. We conclude that arterial vasodilation by a calcium antagonist causes less sympathetic activation than caused by a classical arterial vasodilator. However, during short-term therapy in patients already on a diuretic and a beta blocker, nifedipine appears not to improve decreased LV diastolic function.
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PMID:Effects of nifedipine versus hydralazine on sympathetic activity and cardiac function in patients with hypertension persisting on diuretic plus beta-blocker therapy. 198 Oct 20

The effects of the vasodilator drugs hydralazine, labetalol, prazosin, and nitrendipine were studied on responses to K+ (124 mmol/L), noradrenaline, vasopressin, and angiotensin II in small human maternal intramyometrial arteries and on responses to K+, prostaglandin (PG) F2 alpha, and angiotensin II in fetal stem villous arteries. The vessels were dissected from biopsy specimens obtained during term cesareans and mounted in organ baths. Hydralazine failed to inhibit responses to any of the agonists tested in the fetal and maternal arteries. Labetalol and prazosin decreased responses to noradrenaline but did not affect contractions induced by the other agonists in maternal arteries. In fetal arteries, which did not respond to noradrenaline, no effects of labetalol and prazosin were found. Nitrendipine inhibited responses to all the agonists tested in maternal arteries. In fetal preparations, the drug decreased responses to K+ and PGF2 alpha but did not affect contractions induced by angiotensin II. Vasodilator drugs applied for treatment of pregnancy-induced hypertension show differential effects on human maternal and fetal uteroplacental arteries, depending on their mode of action and the agonists responsible for the contractile activation in these vessels.
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PMID:Effects of vasodilators on isolated human uteroplacental arteries. 201 93

Angiotensin II, when given in low doses, raises blood pressure slowly. When tested in vitro on vascular smooth muscle cells, it has mitogenic and trophic effects; it is not known if it has these effects in vivo. Our purpose was to determine whether vascular hypertrophy develops during slow pressor infusion of angiotensin II and, if so, whether it is pressure induced. Three experiments were done in rats infused subcutaneously with angiotensin II (200 ng/kg/min) by minipump for 10-12 days. Experiment 1: Angiotensin II gradually raised systolic blood pressure (measured in the tail) from 143 +/- 2 to 208 +/- 8 mm Hg (mean +/- SEM), significantly suppressing plasma renin and increasing threefold (NS) plasma angiotensin II. There was no loss of peptide in the pump infusate when tested at the end of the experiment. Experiment 2: In the perfused mesenteric circulation, vasoconstrictor responses to norepinephrine, vasopressin, and KCl were enhanced in rats given a slow pressor infusion of angiotensin II, but sensitivity of responses was not altered. This combination of changes suggests that vascular hypertrophy develops during slow pressor infusion of angiotensin II. Experiment 3: Vessel myography was done after angiotensin II infusion with and without a pressor response. Angiotensin II raised systolic blood pressure, increased heart weight, and produced myographic changes of vascular hypertrophy in the mesenteric circulation, increasing media width, media cross-sectional area, and media/lumen ratio. Hydralazine given with angiotensin II prevented the rise of pressure and the cardiac effect but not the vascular changes. Two-way analysis of variance showed that angiotensin II significantly increased media width, media cross-sectional area, and media/lumen ratio, all independent of hydralazine. Thus, although hydralazine inhibits the pressor and cardiac effects of angiotensin II, suggesting a pressor mechanism for the cardiac change, it does not inhibit structural vascular change, which suggests that at least part of the effect has a non-pressor mechanism.
Hypertension 1991 May
PMID:Angiotensin II causes vascular hypertrophy in part by a non-pressor mechanism. 202 7

Hypertension complicates approximately 10 per cent of all pregnancies and accounts for 20% of all maternal deaths. Blood pressure normally decreases in the first trimester of pregnancy, secondary to a decrease in peripheral vascular resistance, reaches its lowest point in the second trimester and then gradually increases to or near pregravid levels at term. Normal pregnant women develop vascular resistance to the pressor effect of angiotensin II, which is precociously lost in women who develop gestational hypertension. Prostaglandins seem to be involved in the development of this vascular refractoriness. An acute and reversible lesion--defined "Glomerular endotheliosis"--has been described as the basic pathologic pattern of pre-eclamptic nephropathy, although gestational hypertension can be superimposed on undiagnosed essential hypertension or any of a variety of renal diseases. The primary goal when treating gestational hypertension is successful termination of the pregnancy with the least trauma to mother and fetus. Antihypertensive drugs could be administered to prolong pregnancy when this is considered desirable, although pharmacological therapy of gestational hypertension remains a subject for dispute, because of the lack of closely controlled studies. Hydralazine and methyldopa are drugs with a long history of use in gestational hypertension. Beta-blockers have been shown to be as effective as methyldopa. Clinical experience with nifedipine is limited, but controlled clinical trials, currently in progress, suggest its suitability.
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PMID:[Arterial hypertension and the kidney in pregnancy]. 213 37


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