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

The aim of the study was the comparison of the effect of seven day treatment with nifedipine (2 x 10 mg daily) and subsequently with verapamil (3 x 40 mg daily) on blood pressure, heart rate, plasma ANP, cGMP, renin activity (PRA), aldosterone (ALDO) concentrations in patients with primary hypertension. The material consisted of 12 untreated patients with primary arterial hypertension Io WHO. These results suggest that short-term treatment with nifedipine and subsequently with verapamil in patients with primary hypertension Io WHO not influence on plasma ANP, cGMP, PRA and ALDO in spite of blood pressure reduction and the changes in heart rate. It seems that ANP did not participate in hypotensive action of nifedipine and verapamil. No augmentation of urinary sodium excretion was found after short-term treatment with nifedipine or verapamil.
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PMID:[Comparison of the effect of short-term treatment with nifedipine and verapamil on blood pressure, plasma atrial natriuretic peptide (ANP) and cyclic guanosine monophosphate (cGMP) in patients with primary arterial hypertension I degree according to WHO]. 786 84

1. Lungs can take up from the vasculature, circulating forms of atrial natriuretic peptide (Turrin and Gillis, 1986, 1987) and also to synthesize ANP. 2. The lung peptide directly delivered by lungs into the lung vasculature could play a role in the local water/electrolytic balance. 3. Using Spontaneously Hypertensive Rats (SHR), isogenic normotensive controls, the Wistar-Kyoto strain (WKY), and the regular Wistar strain as second control (W), and using a highly sensitive RIA, we measured the immunoreactive IR-ANP content of extracted plasma, lung homogenate and lung perfusate, since there are references of altered ANP levels in this kind of hypertension. 4. The IR-ANP measured in the lung vasculature effluent collected throughout 32 min of Krebs perfusion, was significantly different in all of the three analyzed strains (SHR > WKY > W). 5. The results support the idea of a local function for the peptide hormone directly delivered into the lung vasculature of SHR, which could represent a local adaptation to haemodynamics SHR characteristics besides a genetic characteristic distinguishing WKY from W strains.
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PMID:Generation of atrial natriuretic peptide (ANP) in perfused lungs of spontaneously hypertensive rats (SHR). Comparison to Wistar-Kyoto (WKY) and Wistar (W) rat strains. 809 77

The mechanism of hypoxic moderation of systemic systolic blood pressure was investigated in spontaneously hypertensive rats (SHR). Male SHR rats were divided into hypoxic (H, 5000 m for 15 d) and normoxic (N) groups. The systemic blood pressure of SHR-H (24.9 +/- 1.2 kPa) was found to be 3 kPa lower than that in SHR-N (27.0 +/- 1.3 kPa) (P < 0.05). This protective effect may have been related to the adaptive changes in vascular reactivity which manifested as an increase in the relaxation response of the aorta to ACh (P < 0.01) and a drop in its contraction in response to 5-HT (P < 0.05) following hypoxic exposure. The hypoxic moderating effect against the development of systemic hypertension may have also been related to the increased plasma levels of ANP observed.
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PMID:The hypoxic moderation of systemic hypertension in spontaneously hypertensive rats. 814 25

Cultured rat vascular smooth muscle cells (VSMCs) possess receptors for potent vasoconstrictor endothelin-1 (ET-1) as well as potent vasodilator natriuretic peptides (atrial, brain, and C-type natriuretic peptides [ANP, BNP, and CNP, respectively]). However, little is known about molecular interactions between endothelin receptors and natriuretic peptides in VSMCs. To elucidate whether natriuretic peptides regulate vascular endothelin receptors, we studied the effects of three natriuretic peptides on the capacity of 125I-ET-1 binding and expression of endothelin type A (ETA) and type B (ETB) receptor mRNAs in cultured rat VSMCs. CNP (10(-6) mol/L) increased 125I-ET-1 binding capacity in a time-dependent manner (6 to 48 hours) and stimulated cyclic GMP (cGMP) generation in a dose-dependent manner (10(-8)) to 10(-6) mol/L). Pretreatment with CNP (10(-8) to 10(-6) mol/L) and 8-bromo-cGMP (10(-5) to 10(-3) mol/L) for 24 hours resulted in dose-dependent increases in 125I-ET-1 binding in VSMCs. The three natriuretic peptides at the highest concentration (10(-6) mol/L) increased 125I-ET-1 binding and stimulated cGMP generation with almost the same rank order of efficacy (CNP > BNP > ANP). Scatchard analysis of binding studies revealed that CNP (10(-6) mol/L) and 8-bromo-cGMP (10(-3) mol/L) increased vascular endothelin receptor number by 28% and 88%, respectively, without changing its affinity. Pretreatment with both CNP and 8-bromo-cGMP increased ET-1-stimulated inositol 1,4,5-trisphosphate formation.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1994 Jun
PMID:C-type natriuretic peptide upregulates vascular endothelin type B receptors. 820 31

The present study was aimed to determine the effect of caffeine on the development of renal hypertension. Two-kidney, 1-clip (2K1C) hypertension and deoxycorticosterone acetate (DOCA, 200 mg/kg, subcutaneous implantation)-salt (0.9% NaCl drinking) hypertension were instituted in Sprague-Dawley rats. They were then grouped into two groups each: one was supplemented with caffeine (0.1%) in their drinking solution and the other was not. Systolic blood pressure was measured up to 24 days. Caffeine exacerbated the development of 2K1C hypertension in association with a higher plasma renin concentration (PRC). Caffeine ingestion, however, did not exacerbate but ameliorated DOCA-salt hypertension in which PRC was comparable between the caffeine-ingested and control groups. Concentrations of plasma atrial natriuretic peptide (pANP) were significantly different between the caffeine-ingested and control groups neither in 2K1C nor in DOCA-salt rats, suggesting that ANP was not responsible for the modified blood pressure. Acute caffeine infusion (350 micrograms/min, 30 min) in anesthetized normotensive rats caused increases in urinary excretion (volume and sodium) and in PRC without significantly affecting the blood pressure and pANP. These results suggest that caffeine specifically exacerbates 2K1C hypertension through increasing renin release whereas it ameliorates DOCA-salt hypertension possibly through increasing renal excretion.
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PMID:Chronic caffeine ingestion exacerbates 2-kidney, 1-clip hypertension and ameliorates deoxycorticosterone acetate-salt hypertension in rats. 830 20

To elucidate the physiology of active sodium transport (expressed as erythrocytic ouabian-sensitive sodium efflux rate constant = ERCos) in pregnancy and the influence of dietary sodium intake on that transport, active sodium transport was measured in 52 healthy pregnant women in week 16, 20, 24, 28, 32, 36 or week 38 of gestation. ERCos was not influenced by parity, dietary sodium intake or the development of pregnancy-induced hypertension. A statistical significant shift in ERCos was detected between week 24 and week 28 of gestation accompanied by a shift in intracellular sodium content. The meaning of this change in pregnancy remains unsolved, but an influence of ANP through A-II is suggested.
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PMID:Erythrocytic ouabain-sensitive sodium efflux rate constant in pregnancy. 833 35

Effects of caffeine on ambulatory blood pressure, heart rate, renin-angiotensin system, and ANP were studied in patients treated for mild to moderate hypertension in a randomized, double-blind, placebo-controlled, cross-over trial comparing 2 weeks of caffeine-free diet with 2 weeks of regular coffee use. Twenty-three patients (13 men; aged 28-74 years) with treated, mild to moderate essential hypertension and a regular intake of 3-4 cups of coffee daily completed the study. Mean 24-h, day- or night-time ambulatory blood pressure and heart rate were not different between regimens. Nor were there any effects on the renin-angiotensin system while ANP was significantly increased during caffeine intake. Compliance of the dietary regimen was excellent as assessed by serum caffeine concentration measurements. We conclude that habitual coffee drinking did not influence the 24-h blood pressure profiles or cardiovascular hormones in treated hypertensives.
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PMID:Effect of coffee on ambulatory blood pressure in patients with treated hypertension. 846 68

CHF is a common, complex and life-threatening clinical syndrome. It is widely accepted that enhanced peripheral vascular tone plays a major role in the pathophysiology of CHF. Increased activity of the sympathetic nervous system is one of the most important factors responsible for the increased afterload in CHF. This increase in sympathetic activity occurs early in the course of development of CHF. Efferent sympathetic activity is distributed in a non-uniform way in CHF, with significant increases to the heart and kidney but normal activity to some other organs such as the lung. Increased renal sympathetic activity contributes significantly to altered neural haemodynamics, sodium and water retention, and modulation of the actions of other vasoactive hormones. The regional alteration in sympathetic activity may be largely responsible for the changes in resting regional blood flow to different organs in CHF and the maldistribution of blood flow that occurs during the stress of exercise. Disordered function of cardiovascular reflexes is observed in CHF and may contribute to disordered sympathetic function. In CHF there are significant interactions between the sympathetic nervous system and other humoral systems such as the renin-angiotensin system, AVP, ANP, endothelin and renal DA. The various drugs used in the treatment of CHF have different effects on sympathetic activity: digitalis and ACE inhibitors tend to suppress activity while diuretics may have the opposite effect. Following cardiac transplantation, there is a prompt return of sympathetic function towards normal, although the heart may remain significantly denervated for a long time, with gradual reinnervation. Cyclosporin therapy tends to increase sympathetic activity and this may contribute to post-transplant hypertension.
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PMID:Sympathetic dysfunction in heart failure. 848 86

The effects on blood pressure (BP) and heart rate (HR), at rest and during bicycle exercise, of the vascular selective calcium antagonist felodipine, the cardio-selective beta-blocker metoprolol, and of the two drugs in combination, were assessed in a double-blind, three-way cross-over study comprising 23 patients with essential, mild to moderate hypertension. All three treatment regimens were given to each patient in randomised order for 4 weeks after a 4 week placebo run-in period. Felodipine 10-20 mg daily, metoprolol 100-200 mg daily and the combination of felodipine 10-20 mg plus metoprolol 100 mg daily were all effective antihypertensive treatments both at rest and during exercise. The two drugs seemed to have additive effects and the effect on BP of the combination was greater than that of either drug given as monotherapy. The mean sitting BP was 148/103 mmHg at randomisation, after 4 weeks of placebo treatment, and 134/88, 134/94 and 121/84 mmHg, respectively, after 4 weeks' treatment with felodipine, metoprolol and the combination. Maximal exercise capacity was similar irrespective of treatment regimen, and the normal response to exercise BP and HR was maintained during all active treatments. Changes observed in volume regulatory hormones (PRA, aldosterone and ANP) were consistent with a direct tubular natriuretic-diuretic effect of felodipine and of beta-blocker attenuated release of renin. All treatment regimens were well tolerated and adverse events reported were usually mild and transient.
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PMID:Effects of felodipine, metoprolol and their combination on blood pressure at rest and during exercise and on volume regulatory hormones in hypertensive patients. 853 52

Antihypertensive treatments were given to young and adult SHRs, to prevent and reverse hypertension, respectively. Cardiac hypertrophy and the steady state level of the "fetal" genes, ANP, alpha-skeletal actin (alpha-skA), and beta myosin heavy chain (beta-MHC) mRNAs were assessed. Our findings show that the reduction of blood pressure does not consistently result in a similar regression of the "fetal gene program".
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PMID:Molecular manifestations of cardiac hypertrophy in the spontaneously hypertensive rat effects of antihypertensive treatments. 854 Mar 96


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