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

Hypertension-associated growth of vascular smooth muscle cells might be mediated in vivo by platelet-derived growth factor (PDGF). Our previous investigations in hypertensive rats failed to demonstrate changes in aortic steady-state mRNA levels of PDGF A or B chains. The current studies were performed to determine whether hypertension might affect the expression of PDGF receptors. We studied PDGF alpha- and beta-receptor gene expression by Northern analysis using human and rat cDNA probes. Studies of tissue distribution revealed that PDGF beta-receptor mRNA was most abundant in total aorta and aortic media, whereas the PDGF alpha-receptor mRNA was most abundant in the lung and was expressed at low levels in aortic tissue. Deoxycorticosterone acetate (DOCA)-salt hypertension induced a threefold increase in aortic steady-state PDGF beta-receptor mRNA levels. Aortic PDGF beta-receptor expression also was higher in spontaneously hypertensive rats (SHRs) when compared with age-matched normotensive Wistar-Kyoto (WKY) controls. Aortic PDGF alpha-receptor steady-state mRNA levels were unchanged in DOCA-salt hypertension and were expressed at similar levels in WKY rats and SHRs. Unlike the findings with aorta, cardiac PDGF beta- and alpha-receptor and PDGF B-chain expressions were unchanged in the DOCA-salt model and were decreased in SHRs. These findings indicate that hypertension can increase aortic steady-state mRNA levels for PDGF beta-receptor. They also indicate that tissue-specific expression of the genes of the PDGF ligand/receptor system are differentially regulated in hypertension.
Hypertension 1991 Jun
PMID:Hypertension-induced changes of platelet-derived growth factor receptor expression in rat aorta and heart. 164 70

The importance of the central nervous system (CNS) in the development of mineralocorticoid hypertension has been well documented. Type I receptors in adrenalectomized rats are concentrated in the hippocampus, amygdala, lateral septum, and hypothalamus, particularly in the periventricular regions, areas known to be or suspected of being important in the regulation of ACTH release, arousal, fluid and fluid osmolality equilibrium, and the maintenance of normal blood pressure. In the rat, ablation of the AV3V area and central, but not peripheral, sympathectomy prevent the development of DOCA-salt hypertension. The continuous intracerebroventricular (icv) infusion of aldosterone in rats or dogs at doses which do not affect the blood pressure when administered subcutaneously (sc) produces significant increases in resting blood pressure. In rats this effect is dose dependent, blocked by the concomitant icv infusion of prorenone, an aldosterone antagonist, and enhanced, but not completely dependent upon renal mass reduction and excess salt consumption. The icv infusion of RU28318, a selective mineralocorticoid antagonist, at doses which are ineffective when administered sc, inhibits the development of hypertension produced by the sc infusion of aldosterone or deoxycorticosterone, as well as that produced by the oral administration of a licorice derivative and of a high salt diet in the Dahl S/JR rat. It is assumed that this effect is mediated through the mineralocorticoid receptor because it is inhibited by mineralocorticoid antagonists and because the icv infusion of RU26988, a selective glucocorticoid agonist, has no effect. The concomitant icv infusion of corticosterone, which is thought to be the primary ligand of the brain mineralocorticoid receptor, antagonizes the effect of icv infusion of aldosterone.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:What is the role of the central nervous system in mineralocorticoid hypertension? 164 98

The role of ions and cell membrane function in the pathogenesis of benign and malignant hypertension was investigated in spontaneously hypertensive rats (SHR). Ten-week-old male SHR (n = 50) and SHR treated with deoxycorticosterone acetate (DOCA; n = 70) and 1% NaCl drinking water were studied weekly for 14 weeks. Malignant hypertension developed only in DOCA-salt SHR and was characterised by severe hypertension, failure to thrive and renal fibrinoid necrosis. Fourteen DOCA-salt SHR and one SHR died. Extracellular (serum) and intracellular (erythrocyte and muscle) Na+, K+, Mg2+, Ca2+ and muscle membrane Na+,K(+)-adenosine triphosphatase (ATPase), Ca(2+)-ATPase and Mg(2+)-ATPase were measured at various stages in the development of malignant hypertension. Three developmental phases were defined: benign, premalignant and malignant. DOCA-salt SHR showed persistent hypokalaemia. In the benign phase, there were no differences in Na+, Mg2+ and Ca2+ between SHR and DOCA-salt SHR. In the premalignant phase, serum and erythrocyte Mg2+ and ATPase activity were significantly lower in DOCA-salt SHR compared with SHR. During the late premalignant and malignant phases, intracellular Ca2+ and Na+ were significantly higher in the DOCA-salt SHR compared with SHR. In view of these findings, the abnormalities in DOCA-salt SHR during the early phases of blood pressure elevation could be contributory factors to the development of malignant hypertension.
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PMID:Altered cations and muscle membrane ATPase activity in deoxycorticosterone acetate-salt spontaneously hypertensive rats. 165 84

The activity of sodium-potassium pump was studied in mesenteric arteries and veins of rats, as well as its inhibition effect upon catecholamine-induced contractile responses and the time of relaxation of these vessels in normal rats and in those with DOCA-salt hypertension. The activity was measured by 86Rb [correction of 86Rh] up-take. A difference in the ouabain-sensitive take-up was found between arteries and veins. It was higher in normotensive rats' veins than in arteries; in hypertension, the activity of the pump tended to decrease in arteries and sharply increased in veins. Inhibition of the pump with ouabain reduced arteries' contractile responses to noradrenaline and phenylephrine in normotensive animals, whereas in hypertension the effect involved all the types of stimulation leaving intact the contractions of venous vessels. Ouabain increased the period of relaxation of arteries and veins in some types of stimulation in normal as well as in hypertensive rats.
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PMID:[The activity of the sodium-potassium pump of the mesenteric arteries and veins in normal rats and in DOCA-salt hypertension]. 166 90

We studied the effect of indole-3-pyruvic acid (IPA) on systolic blood pressure of normotensive, spontaneously hypertensive, DOCA + salt hypertensive, and Grollman hypertensive rats. Experiments were also carried out in order to investigate whether IPA may influence the development of hypertension in spontaneously hypertensive rats. Age-matched normotensive, spontaneously hypertensive, DOCA + salt hypertensive, and Grollman hypertensive rats treated with N-methylglucamine, were used as controls. Acute oral (up to 50 mg/kg) and intravenous (5 mg/kg) administration of IPA did not change systolic blood pressure in any models of hypertension. By contrast, a repeated administration of IPA (100 mg/kg/day, by oral gavage for 10 days) significantly decreased systolic blood pressure in all models of hypertension, while it elicited no significant effect in normotensive rats. Moreover, when IPA was given daily to 5-week-old spontaneously hypertensive rats for 7 weeks, it partially inhibited the development of hypertension. In addition, chronic administration of IPA caused enhanced levels of tryptophan and 5-hydroxyindoleacetic acid in the cortex and diencephalon. Brainstem serotonin content in both normotensive and spontaneously hypertensive rats was also enhanced by IPA treatment. Our results suggest that IPA lowers blood pressure in different rat models of hypertension and this effect seems to be correlated with an increase in cerebral serotonin metabolism.
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PMID:Antihypertensive activity of indolepyruvic acid: a keto analogue of tryptophan. 168 65

The specific neutral endopeptidase (NEP) inhibitor, SQ 29,072 (7-[2-(mercaptomethyl)-1-oxo-3-phenylpropyl]amino]heptanoic acid), was studied in conscious spontaneously hypertensive rats (SHRs) and in DOCA/salt hypertensive rats during inhibition of angiotensin-converting enzyme (ACE) activity with captopril or SQ 27,519 (the free acid of fosinopril). In the SHR, the maximal depressor responses to the combination of SQ 29,072 and SQ 27,519 (-44 +/- 4 mm Hg) were greater than the responses to any of the inhibitors given alone (-26 +/- 5, -40 +/- 10, and -28 +/- 6 mm Hg for SQ 29,072, captopril, and SQ 27,519, respectively). In contrast, the maximal antihypertensive activities of SQ 29,072 were the same in conscious DOCA/salt hypertensive rats infused with saline, captopril, or SQ 27,519 (-54 +/- 10, -51 +/- 8, and -58 +/- 11 mm Hg, respectively), indicating a lack of synergism in this model. In agreement, SQ 28,133 [N-[2-(mercaptomethyl)-1-oxo-3-phenylpropyl]-L-leucine], a compound that inhibits both NEP and ACE, elicited significant depressor activities in both SHR and DOCA/salt hypertensive rats. In conclusion, a selective NEP inhibitor enhanced the depressor activity of ACE inhibitors in the conscious SHR, indicating that these agents may be effectively combined for treatment of some types of hypertension.
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PMID:Antihypertensive activity during inhibition of neutral endopeptidase and angiotensin converting enzyme. 171 8

Renal hypertension has been reduced to normal levels in the rat with subcutaneous injections of carbon tetrachloride (CCl4). Previous light microscopic evaluation of liver sections demonstrated varying degrees of hepatocellular and hepatic parenchymal injury secondary to CCl4 administration. In normotensive rat populations, saline injections have been shown not to cause hypertension, and the treatment of normal rats with subcutaneous CCl4 did not change their blood pressure over that of noninjected controls. In this study we compare the extent of blood pressure reduction with the degree of CCl4-induced liver injury in the renal-induced, spontaneous hypertensive rat (SHR), and normotensive rat. Statistically significant blood pressure reduction followed CCl4 injection of renal (p less than .01) and SHR (p less than .001) hypertensive animals. The morphological liver injury appeared most sensitively reflected in hepatocellular nuclear atypia. The SHR animals were the most resistant to CCl4 liver damage by chronic CCl4 treatment. There was no measurable effect of CCl4 treatment on the animals as assessed by their activity, rate of development and weight gain. The degree of blood pressure reduction due to CCl4 treatment in the SHR animals was similar to that previously reported in DOCA and renal-induced hypertensive animals.
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PMID:Hepatocellular injury induced by chronic low-dose CCl4 in spontaneous and renal hypertensive rats: a correlation to the reversal of experimental rat hypertensive models. 174 Jul 67

In order to determine whether the expression of parathyroid hypertensive factor (PHF) is secondary to hypertension or whether it is specifically related to low-renin hypertension, PHF levels were measured in DOCA-salt and two-kidney-one-clip (2K-1C) hypertensive rats. Despite equivalent elevations of blood pressure, PHF was detected in the DOCA-salt rats, but not in the 2K-1C rats (17.5 +/- 3.1 mm Hg, P less than .0001 v 0.9 +/- 2.8 mm Hg, P = NS, respectively). Moreover, PHF levels correlated with mean arterial pressure in the DOCA-salt group (r = 0.91, P less than .0001). We conclude that PHF expression is not a secondary phenomenon caused by hypertension, but rather may be causally related to the development of low-renin forms of hypertension.
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PMID:Parathyroid hypertensive factor is present in DOCA-salt but not two-kidney-one-clip hypertensive rats. 174 13

The present study was designed to clarify the role of calcium in suppressed renin release in DOCA-salt hypertension. Rat glomeruli were isolated by the modified Beierwaltes' sieving method. The glomeruli were superfused with Krebs-Ringer solution. Basal levels of renin release were lower in the DOCA-salt hypertensive rats (1.16 +/- 0.27 ng/ATI/hr/hr/10(4) glomeruli, mean +/- SEM, n = 8) than in the control rats (1.92 +/- 0.18, p less than 0.01, n = 8). Perfusion with a calcium free solution containing EGTA and A23187 stimulated renin release in the DOCA-salt hypertensive and control rats. The maximum levels of renin release during the perfusion in DOCA-salt hypertensive rats (1.79 +/- 0.17, n = 8) were lower than those in control rats (10.60 +/- 1.85, p less than 0.01, n = 8). These results suggest that high levels of intracellular calcium might not contribute to the suppression of renin release in DOCA-salt hypertension.
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PMID:Altered renin release from isolated superfused rat glomeruli in DOCA-salt hypertensive rats. 176 Aug 88

Several lines of evidence suggest that hypertension is a contributing factor to diabetic nephropathy, a major cause of mortality in diabetes mellitus patients. The present study tested the hypotheses (1) that insulin dependent diabetes (IDD) causes hypertension, and (2) that simultaneous hypertension and IDD causes greater renal damage than would be expected from the independent contributions of each disease. IDD was induced by injection of streptozotocin (STZ, 65 mg/kg i.p.) into male Wistar rats, causing severe hyperglycaemia within 4 days. Seven days after the STZ treatment, hypertension was initiated by subcutaneous implantation of deoxycorticosterone acetate and administration of 1% saline in the drinking water (DOCA-NaCl). IDD rats not receiving DOCA-NaCl displayed a small elevation of blood pressure one week after STZ treatment, but thereafter displayed significant hypotension. The IDD rats receiving DOCA-NaCl displayed elevated systolic arterial pressure throughout the study, but by the end of the experiment, their mean systolic arterial pressure was significantly lower than that of the rats treated with DOCA-NaCl alone. Only the IDD/DOCA-NaCl rats displayed significant signs of renal dysfunction, i.e. greatly increased proteinuria and morphological renal damage, including marked distension of distal tubules and occasional casts. No other group displayed these abnormalities.
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PMID:Effects of simultaneous diabetes and hypertension in an insulin dependent diabetic model. 176 11


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