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

If a hypertensive patient with renal artery stenosis (RAS) is to benefit from percutaneous transluminal renal angioplasty (PTRA) in terms of a sustained improvement in blood pressure control, one may postulate a demonstrable reduction in renal blood flow (RBF) to that kidney, reversible by PTRA. In a population of 32 hypertensive patients, RAS was present in 23 of 62 kidneys. Eleven of the 32 patients underwent renal revascularization, of whom 6 showed improvement in blood pressure control at 6 mo, i.e., had renovascular hypertension (RVH). There was no correlation between RBF and angiographic appearances of the renal artery. Furthermore, there was no significant difference between RBF in the stenosed kidneys of the patients with RVH compared with the stenosed kidneys of patients without RVH. Individual kidney RBF was 22% (s.d. 11) higher 1-3 wk after PTRA but the increase did not correlate with clinical outcome. Angiotensin converting enzyme (ACE) inhibition increased RBF by 25% (s.d. 25) of baseline flow before PTRA but the increase did not correlate with clinical outcome. Measurement of RBF is of limited value for the prediction of the long-term blood pressure response following PTRA.
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PMID:Noninvasive measurement of renal blood flow with technetium-99m-DTPA in the evaluation of patients with suspected renovascular hypertension. 226 97

1. Angiotensin II (ANG II) and atrial natriuretic peptide (ANP) are functionally antagonistic circulating hormones involved in blood pressure and body fluid regulation. An inappropriate atrial secretion of ANP has been implicated in the pathogenesis of hypertension, but clinical and experimental results on the role of ANP in hypertension are still conflicting. 2. In the brain both peptides have been localized in close proximity, preferentially in areas involved in central cardiovascular, electrolyte and volume control. ANP was shown to inhibit ANG II-induced drinking, release of pituitary hormones and natriuresis, and to induce sodium retention when given alone. 3. These findings suggest that also in the brain ANG II and ANP exert functionally antagonistic effects. However, in contrast to their peripheral effects, ANG II induces natriuresis while ANP appears to cause antinatriuresis in the brain.
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PMID:Atrial natriuretic peptide (ANP) as a neuropeptide: interaction with angiotensin II on volume control and renal sodium handling. 214 93

Left ventricular hypertrophy is an adaptation of the cardiac fibre to the imposed mechanical overload. This adaptation is quantitative; increased numbers of contractile units with decreased wall stress. Qualitative changes in genomic expression allow the hypertrophied cardiac fibre to develop a normal active tension at the expense of its maximal shortening velocity. These changes are preceded by the temporary expression of proto-oncogenes, of genes of the proteins of thermal shock and by reorganisation of the cytoskeleton, all possible candidates of the regulation of the gene expression in cardiac hypertrophy. In the long-term, the hypertrophy becomes harmful: inadequate subendocardial vascular development; the lowering of the Vmax is beneficial at cellular level but eventually affects cardiac output; ventricular compliance decreases with the development of fibrosis; changes in calcium metabolism are arrhythmogenic. Modifying, prolonging and improving the natural process of adaptation is clearly the first therapeutic objective in order to decrease the hypertension and cause the hypertrophy to regress. Propranolol acts by reducing the cardiac work load. However, betablockers have the disadvantage of increasing the relative density of the subendocardial collagen. Rilmenidine decreases the quantity and density of the collagen. Vasodilators and diuretics induce regression of the myocytic hypertrophy by lowering the threshold of adaptation of these cells, but they have no effect on collagen synthesis. Angiotensin converting enzyme inhibitors which have been shown to be beneficial in controlling hypertension, induce a decrease in the hypertrophy of the myocytes and reduce fibrosis.
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PMID:[Remission of left ventricular hypertrophy of hypertensive origin. Experimental data]. 215 Apr 72

Although alterations in Ca2+ metabolism have been demonstrated in subcultured aortic myocytes of spontaneously hypertensive rats (SHR), changes in intact tissue have not been described. This study compares Ca2+ metabolism in intact mesenteric resistance arteries and in myocytes that were derived from mesenteric arteries and maintained in primary and long-term culture. Using fura-2, basal levels of Ca2+ were found to be similar in intact vessels of SHR and Wistar-Kyoto normotensive rats (WKY), and in primary and first-passage myocytes of the two strains. During subculture, basal levels of Ca2+ became elevated in myocytes of SHR. When norepinephrine-induced Ca2+ mobilization was examined, the threshold of resistance arteries was lower in SHR, but differences were not detected with higher concentrations of the agonist. Norepinephrine-induced Ca2+ mobilization also did not differ between primary myocytes of the two strains. Angiotensin II elicited greater intracellular Ca2+ responses in myocytes of SHR at passages 1, 3 and 5. Cell growth was assessed at each passage level. While no strain differences were detected in primary, first- and second-passage cells, the growth rate became elevated in SHR in subsequent passages. These results are consistent with the hypothesis that vascular myocytes cultured from SHR with established hypertension exhibit differences in Ca2+ metabolism that are not present in the intact vessel wall. Furthermore, intracellular Ca2+ appears to be elevated in myocytes of SHR when the rate of proliferation is increased.
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PMID:Intracellular Ca2+ metabolism of isolated resistance arteries and cultured vascular myocytes of spontaneously hypertensive and Wistar-Kyoto normotensive rats. 215 55

Angiotensin converting enzyme (ACE) activity was measured by fluorimetry in the plasma, lung, heart, aorta and kidney (cortex and medulla) of 3-, 5-, 8- and 11-week-old spontaneously hypertensive rats (SHR) and compared with that of age-matched Wistar-Kyoto rats (WKY). In the plasma, lung and kidney (cortex and medulla), ACE activity was lower in SHR than in WKY. This was evident as early as the age of 3 weeks. In contrast, there were no differences between SHR and WKY in the aorta and the heart. Age-related variations in ACE activities differed in each tissue and in both groups of rats, but no major modifications were correlated with the development of hypertension. A binding assay was performed with [3H]ramiprilat; affinity (KD) and the maximum number of binding sites (Bmax) were determined in plasma and tissues of 3-week-old SHR and WKY. The KD values were identical in the two groups but Bmax was lower in all SHR tissues except in the heart; these results might be related to the decrease in ACE activity. Our results probably reflect genetic differences in ACE activity between SHR and WKY, and suggest that ACE regulatory mechanisms act differently in each tissue.
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PMID:Age-related variations in tissue angiotensin converting enzyme activities: comparison between spontaneously hypertensive and Wistar-Kyoto rats. 217 May 8

The reaction of the renin-angiotensin system to acute angiotensin converting enzyme inhibition was investigated in a single-blind, crossover study in nine normal volunteers receiving two out of three regimens in random order: the new converting enzyme inhibitor benazepril (20 mg once or 5 mg four times at 6-hour intervals) or enalapril (20 mg). Plasma converting enzyme activity, drug levels, angiotensin I and angiotensin II, active renin, and aldosterone were measured before and 1-4 hours and 14-30 hours after drug intake. Baseline in vitro plasma converting enzyme activity was 97 +/- 15 nmol/ml/min (mean +/- SD) when Hip-Gly-Gly was used as substrate, but with carbobenzoxy-Phe-His-Leu (Z-Phe-His-Leu) or angiotensin I as substrate it was only 20 +/- 4 and 1.7 +/- 0.3 nmol/ml/min, respectively. Discriminating power at peak converting enzyme inhibition was enhanced with the two latter substrates. In vivo converting enzyme activity was estimated by the plasma angiotensin II/angiotensin I ratio, which correlated well with in vitro converting enzyme activity using Z-Phe-His-Leu as substrate (r = 0.76, n = 252). Angiotensin II levels returned to baseline less than 24 hours after drug administration, whereas in vitro and in vivo converting enzyme activity remained considerably inhibited and active renin together with angiotensin I levels were still elevated. A close linear relation was found between plasma angiotensin II and the angiotensin I/drug level ratio (r = 0.91 for benazeprilat and r = 0.88 for enalaprilat, p less than 0.001). Thus, plasma angiotensin II truly reflects the resetting of the renin-angiotensin system at any degree of converting enzyme inhibition. The ratio of plasma angiotensin II to angiotensin I represents converting enzyme inhibition more accurately than in vitro assays, which vary considerably depending on substrates and assay conditions used.
Hypertension 1990 Nov
PMID:Determinants of angiotensin II generation during converting enzyme inhibition. 217 61

Angiotensin converting enzyme (ACE) activity in the endothelium and smooth muscle cum adventitia of the normo- and hypertensive rat aorta was investigated. The aortic tissues of spontaneously hypertensive (SHR) rats, compared to those of the Wistar Kyoto (WKY) and Sprague Dawley (SD), contained significantly higher level of ACE activity. Expressed as mumole per min per mg total protein, the endothelium of the SHR contained 105 +/- 11 (mean +/- SEM) and those of the WKY and SD, 69 +/- 7 and 77 +/- 9, respectively. Similarly, the ACE activity in the smooth muscle cum adventitia were 97.6 +/- 8.2, 52.6 +/- 6.4 and 25.7 +/- 4.1 for the SHR, WKY and SD respectively. These results support our earlier assumption that the high level of ACE activity in the lung of SHR is a reflection of the increase in ACE activity of the blood vessels. However, our results and related findings of other investigators do not permit firm speculation as to whether the increase in ACE activity in the SHR is the cause or the result of hypertension in these animals.
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PMID:Angiotensin converting enzyme in the endothelium and smooth muscle cum adventitia of the normo- and hypertensive rat aorta. 217 83

Hypertensive subjects who have received no treatment have been found to be hyperinsulinaemic in previous studies using different populations. The present study was carried out to further examine the metabolic disturbances in carefully treated hypertensive subjects [diastolic blood pressure (DBP) less than 90 mmHg] of both sexes from the Dalby population. Three hundred and ten subjects who had been hypertensive for more than 5 years [DBP 88.1 +/- 0.5 (mean +/- s.e.m.)] were compared with 288 normotensive controls, matched for sex and age and chosen from the same population. After an overnight fast and with no medication for 24 h, an oral glucose tolerance test was carried out. P-insulin and P-C-peptide were analysed and insulin sum (P-insulin at start + after 2 h of oral glucose tolerance test) and C-peptide sum were calculated. Insulin and C-peptide sums were higher (P less than 0.001) in the hypertensive than in the normotensive subjects; 0.69 +/- 0.03, 3.36 +/- 0.08 and 0.41 +/- 0.02, 2.74 +/- 0.06, respectively. The diagnosis of hypertension, not the attained blood pressure level, correlated with insulin and C-peptide sums in multivariate analyses; F-values 20.96 (n = 598; P less than 0.001) and 6.68 (P less than 0.01), respectively. Hypertensive subjects under treatment, using calcium antagonists as monotherapy (n = 21), did not differ in age or body mass index from other hypertensives, but they had lower values for insulin and C-peptide sums; 0.45 +/- 0.05 and 2.63 +/- 0.18. Angiotensin converting enzyme inhibitors were not frequently used for monotherapy.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hyperinsulinaemia and other metabolic disturbances in well-controlled hypertensive men and women: an epidemiological study of the Dalby population. 217 49

Angiotensin II has recently been shown to exert potent control over sodium and water absorption in the proximal convoluted tubule. This transport stimulation is effected by receptors on both the luminal and basolateral membranes of cells located predominantly in the early, S1 proximal tubule. Angiotensin II increases transport primarily by a Gi protein-mediated reduction in intracellular cyclic adenosine monophosphate, which enhances the affinity of the Na(+)-H+ antiporter. Change in early proximal acidification ultimately causes alteration in the amount of sodium chloride leaving the proximal tubule and entering the urine. These direct tubular transport actions by angiotensin II may participate importantly in various physiological actions of the kidney, including the renal response to change in dietary sodium intake and in extracellular volume, as well as in pathophysiological processes such as hypertension.
Hypertension 1990 May
PMID:Angiotensin II: a powerful controller of sodium transport in the early proximal tubule. 218 49

Angiotensin converting enzyme inhibitors (ACEI) are used widely in the treatment of both hypertension and congestive heart failure. Although usually well tolerated, these medications may produce side effects that may be encountered by the allergist, including cough, angioedema, and rhinitis symptoms. The severity of ACEI-induced cough may vary, and is associated with increased bronchial hyperreactivity in some (but not all) patients as judged by methacholine sensitivity. Angiotensin converting enzyme inhibitor-induced cough may have its onset from one day to 12 months after initiation of therapy, and is not dose dependent. Angioedema caused by ACEI is usually mild and clears with discontinuation of the drug, however cases requiring intubation and tracheostomy have been reported. The mechanism of ACEI-induced cough remains unclear, but could be in part due to accumulation of substances whose degradation may also be impeded by ACEI, such as substance P, bradykinins, and/or prostaglandins. Knowledge of the side effects produced by this class of medication may help patients avoid unnecessary, costly, and often invasive diagnostic evaluations.
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PMID:Angiotensin converting enzyme inhibitors and the allergist. 222 91


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