Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To evaluate neural mechanisms in salt-sensitive hypertension, norepinephrine turnover rates were measured in peripheral tissues and selected brain areas of Dahl salt-sensitive and salt-resistant rats receiving either 1% or 7% NaCl diets for 5 weeks. Norepinephrine turnover was determined by measuring tissue norepinephrine in untreated animals or in separate groups killed 2, 4, 6, and 10 hours after alpha-methyl-tyrosine. Plasma volume (radiolabeled albumin) was also measured. Arterial pressure of Dahl S rats receiving 7% NaCl (167 +/- 4 mm Hg) was higher (p less than 0.001) than that of Dahl S rats receiving 1% NaCl (141 +/- 3mm Hg), which was higher (p less than 0.001) than that of Dahl R rats receiving both NaCl intakes. Norepinephrine turnover was increased (p less than 0.01) by 7% NaCl in both heart and brown adipose tissue in Dahl S rats, whereas norepinephrine turnover in Dahl R rats was decreased (p less than 0.01) by the 7% NaCl intake in the heart and kidney. On the high NaCl intake, norepinephrine turnover in heart and adipose tissue was lower (p less than 0.05) in Dahl R rats than in Dahl S rats. In brain stem tissue, with the 1% NaCl diet, norepinephrine turnover was higher (p less than 0.001) in Dahl S rats than in Dahl R rats, and norepinephrine turnover was inhibited (p less than 0.001) by the high NaCl intake in Dahl S rats but not in Dahl R rats. In posterior hypothalamus, norepinephrine turnover was inhibited (p less than 0.01) by the high NaCl intake in Dahl R rats but not in Dahl S rats.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of dietary NaCl on norepinephrine turnover in the Dahl rat. 201 93

Acute reversible renal failure is a widely recognized potential complication of angiotensin-converting enzyme inhibitor (ACEI) administration in renovascular hypertension, particularly in bilateral artery stenosis or stenosis involving a solitary kidney. We report herein 2 cases of a rare but severe complication, i.e., acute renal artery thrombosis. Whereas marked hypotension does not seem to be necessary to trigger acute renal failure following ACE inhibition, by contrast, the fall in blood pressure could play an important role in our patients. Since single-dose ACEI has been advocated in order to improve the predictive value of renal scintigraphy or plasma renin activity measurements in the diagnosis of renovascular hypertension, the potential risk of this approach should be stressed.
Nephron 1991
PMID:Acute renal thrombosis induced by angiotensin-converting enzyme inhibitors in patients with renovascular hypertension. 202 Mar 53

Hypertension caused by deoxycorticosterone-salt (DOC-salt) may involve enhanced sympathetic tone and some diuretics may exert their antihypertensive action by modulating presynaptic adrenergic sensitivity. This study analyzes the noradrenergic sensitivity of the perfused mesentery isolated from DOC-salt hypertensive rats treated or not with chlorthalidone. Chlorthalidone treatment reduced arterial hypertension in DOC-salt treated rats (from 160 +/- 7 to 127 +/- 5 mmHg). The diuretic completely prevented the increase in sympathetic tone and blunted the decreased vagal tone observed in DOC-salt rats. Norepinephrine-induced vasoconstriction was enhanced in perfused mesenteries isolated from DOC-salt rats. This alteration was attenuated in preparations from chlorthalidone-treated DOC-salt animals. Blockade of neuronal catecholamine uptake using cocaine did not change these responses. These data suggest that chlorthalidone reduces the vascular hyperresponsiveness to catecholamines observed in DOC-salt treated hypertensive rats.
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PMID:Chlorthalidone alters the vascular reactivity of DOC-salt hypertensive rats to norepinephrine. 210 Oct 67

To validate a miniature swine model of sympathectomy, six swine that had chronic high blood pressures for unknown reasons and five DOCA hypertensive swine were treated with a single dose of the neurotoxin 6-hydroxydopamine (6-OHDA) (50 mg/kg i.v.). One week after 6-OHDA, conscious mean arterial pressure (MAP) had fallen by 47-49 mmHg and the pressor response to tyramine was attenuated in both groups. Norepinephrine content was significantly decreased in the kidneys (greater than 85%) and left ventricle (greater than 94%) in both 6-OHDA treated groups. These results indicate that 6-OHDA can be used to effectively sympathectomize adult swine. Chemical sympathectomy of swine with either unexplained high blood pressure or experimentally induced DOCA hypertension resulted in an equivalent fall in MAP in both of these populations. Further studies using 6-OHDA in miniature swine may help to elucidate the mechanisms involved in maintaining hypertension in this animal model.
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PMID:Effects of 6-hydroxydopamine in hypertensive adult miniature swine. 211 51

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

In order to investigate the involvement of endothelium-derived vasoactive substances in deoxycorticosterone acetate (DOCA)-salt hypertension, the responses to noradrenaline, acetylcholine, sodium nitroprusside and papaverine were studied in the absence and presence of indomethacin. Noradrenaline was equally effective in evoking a constrictor response of aorta, with or without endothelium, isolated from DOCA-salt hypertensive rats, while in controls, noradrenaline induced higher submaximal responses in rubbed than in unrubbed preparations. A decreased response to acetylcholine, an endothelium-dependent vasodilator, was observed in aorta with endothelium which had been precontracted with noradrenaline isolated from hypertensive rats. The relaxant response was lost after removal of the endothelium in both control and DOCA-salt hypertensive groups. The response to sodium nitroprusside, an endothelium-independent agent, in aorta isolated from hypertensive rats as well as the response to papaverine, an agent partially dependent on the endothelium, was not altered. Indomethacin treatment altered the response to noradrenaline only in unrubbed aorta of hypertensive rats. In these preparations, a biphasic response to noradrenaline was observed. At lower concentrations noradrenaline induced the characteristic constrictor response, while at higher concentrations a relaxant response was obtained that was abolished by methylene blue, a guanylate cyclase inhibitor. This could indicate that noradrenaline induced the release of endothelium-derived relaxing factor (EDRF) in aorta of hypertensive rats. Furthermore, indomethacin treatment restored the decreased response to acetylcholine in aorta isolated from DOCA-salt hypertensive rats.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Indirect evidence for an endothelium-derived contracting factor release in aorta of deoxycorticosterone acetate-salt hypertensive rats. 215 57

The antihypertensive and renal effects of the angiotensin-converting enzyme inhibitor lisinopril were studied in a group of patients with moderate-to-severe hypertension and impaired renal function. After 12 weeks of treatment, most patients had good blood pressure response to lisinopril monotherapy. During this period, correlations between antihypertensive effect, drug dose, and serum drug level were observed. These correlations were no longer evident after prolonged treatment. During a 1-year follow-up period, the drug dose was lowered gradually without losing antihypertensive effect. Hyperkalemia occurred in one third of the patients. During the 1-year follow-up, the glomerular filtration rate (GFR) decreased in two thirds of the patients and remained stable in the other third. In this latter group, the pretreatment GFR was higher, and the effective renal plasma flow had increased, whereas in the patients with a decreased GFR no renal vasodilation had occurred during lisinopril therapy. Thus, lisinopril is an effective antihypertensive drug for patients with impaired renal function. The dose should be adjusted to the pretreatment GFR, and a decrease in dosage should be considered with prolonged treatment.
Nephron 1990
PMID:Lisinopril in hypertensive patients with renal function impairment. 216 Oct 83

This is a review of selected aspects of hypertension in infants and children. The causes of pediatric hypertension are discussed. The role of diet in the etiology and/or treatment of hypertension is examined. Following a discussion of the morbidity and mortality of hypertension, aspects of the treatment of chronic hypertension are presented. Finally, a series of patients seen by our service with malignant hypertension is reported.
Nephron 1990
PMID:Hypertension in infants and children. 218 78

Nephron loss is a common progression of a diverse range of kidney diseases. Recent experimental models of chronic renal disease have suggested that hemodynamic and nonhemodynamic mechanisms play key roles in progressive renal injury. Extensive renal ablation in the rat was followed by development of altered glomerular hemodynamics. Albuminuria and histologic damage leading to focal glomerulosclerosis were preceded by the development of increased glomerular pressures and were prevented by interventions such as severe dietary protein restriction and angiotensin-converting enzyme (ACE) inhibitor therapy. Both experimental interventions ameliorated glomerular hypertension. It was therefore concluded that these interventions ameliorated injury by glomerular hemodynamic effect. Similar findings were obtained in a rat model of type I diabetes mellitus induced by streptozotocin in which glomerular hemodynamic factors appeared important to the development of progressive renal disease. Recent studies have suggested that nonhemodynamic factors have important roles in the progression of glomerular injury. For example, although the predominant effects of ACE inhibitor therapy appear to be hemodynamically mediated, data are emerging which suggest that these agents may also influence growth/proliferation of glomerular cells. Because hyperplasia/hypertrophy may influence glomerular susceptibility to injury, this may also be a potential mechanism whereby ACE inhibitor therapy influences glomerular damage. In addition, a variety of studies have suggested that hyperlipidemia, which is frequent accompaniment of glomerular disease, is an important modulator of glomerular injury independent of glomerular hemodynamic effects. Coagulation factors, calcium phosphorus balance, as well as the genetic susceptibility of the glomerulus to injury, all appear to contribute to progressive nephron destruction.
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PMID:Renal protective effects of angiotensin-converting enzyme inhibition. 218 11

Angiotensin-converting enzyme inhibitory therapy is widely used to treat hypertension. With long-term use, it is now being shown to have a beneficial effect on renal function and proteinuria in patients with renal insufficiency. When hypertensive patients with renal insufficiency are treated with enalapril, glomerular filtration rate is maintained, effective renal plasma flow is increased, and microalbuminuria and gross proteinuria are reduced. These beneficial renal changes with enalapril therapy differ from those of most other conventional antihypertensive medications. Clinical awareness of potential problems with hyperkalemia and increasing azotemia, particularly in the setting of salt/volume depletion, is important to assure optimal patient management. When these problems occur, they are nearly always reversible by correcting salt/volume status and/or interrupting enalapril therapy.
Nephron 1990
PMID:Long-term renal effects of enalapril therapy in patients with renal insufficiency. 218 74


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