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

The metabolic and haemodynamic effects of elevating plasma calcium levels were examined in both normal and ACTH-hypertensive sheep. Six weeks of dietary Ca++ supplementation did not alter plasma calcium levels, blood pressure or heart rate. Five days of CaCl2 infusion (2 mmol/h) or intravenous vitamin D injections elevated plasma ionised and total Ca++ levels and heart rate but mean arterial pressure was unchanged. As in other species, elevation of plasma Ca++ levels over 4 hours by infusion of CaCl2 at 2, 5, and 10 mmol/h increased mean arterial pressure and decreased heart rate. The course of ACTH-induced hypertension was not altered in animals supplemented with CaCl2 in their drinking water for 6 weeks nor by intravenous injection of vitamin D for 5 days. This study does not support a major role for altered plasma ionised or total Ca++ levels in the genesis of ACTH-dependent hypertension in the sheep.
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PMID:The effects of calcium and vitamin D on blood pressure in conscious sheep. 285 74

Experiments were performed in male Wistar rats with renovascular hypertension (167 +/- 4.2 mmHg) produced by clipping the renal artery for a 3-wk period (2-kidney, 1-clip Goldblatt). The results were compared with those obtained in age-matched normotensive controls. Hypertension of 3-wk duration elicited a significant increase in ventricular weight (1.01 +/- 0.02 g) with respect to the controls (0.82 +/- 0.01 g) but had no significant effect on body weight. The inotropic responsiveness to beta-adrenergic stimulation was diminished in papillary muscles from renal hypertensive rats: the maximum increase in the maximal rate of rise of tension produced by isoproterenol was 27.39 +/- 5.4 and 11.77 +/- 2.91 g X mm-2 X s-1 (P less than 0.05) in control and hypertensive animals, respectively. Similar results were obtained when the estimated maximal velocity of shortening of the contractile element (Vmax) was used to assess myocardial contractility. The inotropic response to CaCl2 was also significantly depressed in the 2-kidney, 1-clip rats. However, the relaxant and the chronotropic responses to isoproterenol were not significantly modified in the Goldblatt rats. Assays of beta-adrenergic receptors to l-[3H]dihydroalprenolol binding, showed no significant changes in the number (expressed per mg of membrane protein) or in the affinity of the beta-receptors. These results suggest that at an early stage of the renal hypertensive model the impaired inotropic response to isoproterenol is not mediated by an alteration of the beta-receptors and should be searched at a postreceptor adenyl cyclase level.
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PMID:Renal hypertension impairs inotropic isoproterenol effect without beta-receptor changes. 299 71

The purpose of the present study was to investigate erythrocyte membrane abnormalities in hypertension by means of an electron spin resonance and spin-label technique. The erythrocytes from spontaneously hypertensive rats (SHR) and humans with untreated essential hypertension were examined and compared with their normotensive counterparts, and electron spin resonance spectra were obtained for a fatty spin-label agent (5-nitroxy stearate) incorporated into the erythrocyte membranes. The value of outer hyperfine splitting (2T' parallel) was significantly higher in erythrocytes of SHR and humans with essential hypertension than in erythrocytes of normotensive controls (at 37 degrees C: SHR, 56.14 +/- 0.51 gauss [G], n = 8; Wistar-Kyoto rats, 52.22 +/- 0.86 G, n = 4, p less than 0.01; humans with essential hypertension, 56.94 +/- 0.27 G, n = 11; normotensive subjects, 55.44 +/- 0.36 G, n = 8, p less than 0.01). The order parameter (S) was also increased in the hypertensive rats and humans compared to their respective normotensive controls. When calcium was loaded to erythrocytes with calcium ionophore A23187 (0.9 microM) and CaCl2 (1.0 mM), the parameters of the spectra were increased. These changes were more prominent in the hypertensive groups than in the normotensive controls. These results revealed that the erythrocyte membranes of the hypertensive subjects tolerated different spin motions than those of the normotensive controls in the electron spin resonance study and that membrane fluidity might be decreased in hypertension. Additionally, calcium loading to erythrocytes caused the reduction of membrane fluidity. Therefore, it is suggested that an abnormality of calcium handling at the cellular level might affect physical properties of the biomembranes in hypertension.
Hypertension 1987 Jun
PMID:Electron spin resonance studies of erythrocytes from spontaneously hypertensive rats and humans with essential hypertension. 303 3

To investigate whether provision of supplemental dietary calcium could attenuate hypertension in the deoxycorticosterone (DOC) model of hypertension we directly measured mean arterial pressure (MAP) in uninephrectomized rats given DOC, a fixed amount of dietary NaCl, and supplemental dietary calcium as CaCO3 or CaCl2. After 4 weeks MAP in rats given 4% dietary calcium as CaCO3 was significantly lower than the in controls given 0.5% calcium as CaCO3. Provision of 2% calcium as CaCO3, however, failed to attenuate hypertension. Provision of just 1% dietary calcium as CaCl2 attenuated hypertension without inducing impaired weight gain or hypophosphataemia. These findings demonstrate that in rats given DOC and NaCl, provision of supplemental dietary calcium can attenuate hypertension. The findings suggest that: (1) the blood pressure response to supplemental calcium can be determined by the anionic component of the calcium salt consumed, and (2) the antihypertensive effect of supplemental calcium is not just a consequence of impaired weight gain or hypophosphataemia.
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PMID:Attenuation of deoxycorticosterone-induced hypertension by supplemental dietary calcium. 347 93

The effects of oral calcium loading on the blood pressure of spontaneously hypertensive rats (SHR) (n = 20) and age-matched normotensive Wistar-Kyoto rats (WKY) (n = 16) were investigated. Calcium loading was performed by adding 1.5% CaCl2 (Calcium chloride) to the drinking water. Calcium loading attenuated the development of hypertension in the SHR but not in the WKY, and at the end of a 3 week experiment, systolic blood pressure was 171+2 vs 197+3 mmHg (P less than 0.01). In spite of this reduction of blood pressure, there were no significant changes in sodium-water balance, plasma levels of norepinephrine and epinephrine, plasma renin activity, plasma aldosterone concentration and serum electrolytes due to the calcium treatment. On this basis, the depressor mechanism of calcium loading in the SHR was studied by observing the pressor response to norepinephrine and the vascular reactivity to norepinephrine in hind limb perfusion. It was found that both the pressor response and the vascular reactivity were significantly attenuated by the calcium treatment in the SHR but not in the WKY. These results suggest that the antihypertensive effects of calcium treatment in SHR may depend mainly on attenuation of the vascular reactivity.
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PMID:Effects of calcium loading on blood pressure in spontaneously hypertensive rats: attenuation of the vascular reactivity. 352 8

Systolic and mean blood pressures were shown to increase from means of 159 +/- 7 and 111 +/- 7 mm Hg to 174 +/- 8 and 122 +/- 6 mm Hg, respectively (p less than 0.05 in each case), after a 2-hour intravenous infusion of CaCl2 during which serum magnesium levels were found to decrease from 1.8 +/- 0.06 to 1.4 +/- 0.05 mg/dl (p less than 0.0005). A significant increase in blood pressure was not seen when MgSO4 was given intravenously concomitantly with the CaCl2 so that serum magnesium levels did not decline. We conclude that hypercalcemic hypertension is due in part to altered serum magnesium and is prevented if serum magnesium is sustained.
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PMID:Magnesium prevents acute hypercalcemic hypertension. 369 13

The association of acute hypercalcaemia with hypertension has long been known. Its mechanism has remained unexplained, however, since no significant pressor contribution from the renin-angiotensin system or the sympathetic nervous system has been detected. To assess the possible contribution of arginine vasopressin (AVP), we investigated the effect of a 2 h infusion of 2 ml isotonic calcium gluconate (0.46 mmol/ml Ca2+) on the mean blood pressure of anephric (n = 8) or intact (n = 7) rats and the blood pressure response to a specific vasopressin inhibitor (V1). In anephric rats, blood pressure rose by 30 +/- 3 mmHg (mean +/- s.e.m.) and plasma AVP levels rose to 34 +/- 9 pg/ml. In response to injection of the AVP inhibitor, blood pressure fell by 26 +/- 3 mmHg. In intact rats, blood pressure rose by 12 +/- 4 mmHg with plasma AVP levels 14.5 +/- 3.2 pg/ml (normal range 2.2 +/- 1.1 pg/ml), but did not respond consistently to AVP inhibition. Serum calcium levels at the end of the infusion were 25.0 +/- 4.3 mg/dl in anephric and 24.9 +/- 1.2 mg/dl in intact rats. In order to confirm that the calcium ion was indeed responsible for the AVP-dependent changes in blood pressure, another group of anephric rats (n = 8) received a 2 h infusion of CaCl2 (0.46 mmol/ml Ca2+) and exhibited a blood pressure rise of 35 +/- 3 mmHg, which responded to the AVP inhibitor with a blood pressure fall of 22 +/- 3 mmHg. Moreover, prior treatment with indomethacin greatly attenuated the pressor effect of calcium infusion and prevented the rise of AVP.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Calcium stimulates vasopressin release. 377 99

The etiology of hypercalciuria remains unknown in spontaneously hypertensive rats (SHR). In order to differentiate absorptive versus renal hypercalciuria, serial measurements of urinary calcium (UCaV) excretion were made weekly under fasting (3-hour urine collection) and after oral administration of CaCl2 (50 mg/100 g; 4-hour urine collection) from age 8 to 14 weeks in SHR (n = 14) and normotensive Wistar Kyoto rats (WKY; n = 14). Fasting UCaV was significantly greater in WKY than in SHR throughout the periods of observation. In contrast, after oral Ca loading UCaV was greater in SHR after 13 weeks of age (13 weeks: SHR UCaV = 954 micrograms/mg creatinine, WKY UCaV = 541 p less than 0.01; 14 weeks: SHR UCaV = 988 micrograms/mg creatinine, WKY UCaV = 534, p less than 0.01). Fasting urinary cyclic adenosine monophosphate (AMP) excretion was not different between WKY and SHR. However, cyclic AMP excretion of SHR, but not WKY, was decreased after calcium loading when compared to the fasting values. The cyclic AMP was also significantly lower in SHR than in WKY rats after calcium loading. Calcium handling by the kidney was not different between SHR and WKY with or without parathyroidectomy. Calcium disposition kinetic studies were performed on these animals at age 15 and 16 weeks. No significant difference of intravenous 45Ca was observed between WKY (n = 6) and SHR (n = 6) in total plasma clearance, nonrenal clearance, biologic half-life, and elimination rate constant from the central compartment. However, the WKY had a significantly greater renal clearance of 45Ca than the SHR (0.48 +/- 0.04 vs. 0.24 +/- 0.02 ml/n, p less than 0.001). Since tissue disposition of intravenous 45Ca was not different between WKY and SHR, the increased renal excretion of calcium after oral administration in SHR, therefore, reflects increased intestinal absorption of calcium. Correction of established hypertension did not abolish the hypercalciuria. We believe that increased gastrointestinal absorption of calcium is responsible for the hypercalciuria in SHR.
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PMID:Pathogenesis of hypercalciuria in spontaneously hypertensive rats. 396 17

Acute hypercalcemia in the conscious, unanesthetized rat, achieved by a 30-minute infusion of CaCl2 (serum calcium level, 12.8 +/- 0.6 mg/dl) resulted in significant elevation of mean arterial pressure (from 112 +/- 2 mm Hg to 129 +/- 3 mm Hg, p less than 0.001). This pressor response was associated with a significant increase in systemic vascular resistance, from 0.45 +/- 0.02 mm Hg/(ml/min)/kg body weight to 0.50 +/- 0.02 mm Hg/(ml/min)/kg body weight (p less than 0.05), but it caused no alteration in cardiac index. The pressor response to acute hypercalcemia does not appear to be mediated by vasopressor hormones or attenuated by vasodepressor hormones since inhibition of the renin-angiotensin system (nephrectomy), catecholamines (central and peripheral 6-hydroxydopamine), vasopressin (vascular antagonist), prostaglandins (indomethacin), and parathyroid hormone (parathyroidectomy) did not significantly alter the pressor response to infusion of CaCl2 in spite of similar serum calcium levels in all groups of animals. Rather, the pressor response to acute hypercalcemia seems to be mediated by a direct action of calcium ion on smooth muscle and perhaps myocardial cell contractility, since pretreatment with the calcium channel blockers verapamil or nifedipine blocked the pressor response to acute hypercalcemia.
Hypertension
PMID:Mechanism of acute hypercalcemic hypertension in the conscious rat. 407 24

Cyclic analogs of bradykinin (CBK) and kallidin (CK) have a weak myotropic activity and a marked and prolonged hypotensive effect unlike linear bradykinin (BK) and kallidin (K) which produce a short-term hypotension and considerable contraction of rat uterus smooth muscles. Myotropic effects of BK and CK were significantly inhibited by phentolamine, methysergide, papaverine and verapamil. Atropine, diphenhydramine and propranolol have no influence on the kinin-induced myotropic responses. The prolonged decrease in blood pressure induced by CBK and CK is observed in un- and anesthetized normotensive, spontaneously hypertensive rats and rats with renovascular hypertension and is absent from anesthetized cats and guinea-pigs. This indicates the species specificity of cyclokinins. Indomethacin, diphenhydramine and methysergide failed to influence the BK- and CK-induced hypotensive effects on anesthetized rats. CaCl2 did not influence the magnitude of the hypotensive effect of BK and CK, however, it significantly shortened the duration of the CK-induced hypotensive effect. In vitro CBK and CK inhibited activity of kininase II in a similar manner (at a concentration range of 10(-5) M) but to a less extent than BK (10(-7)-10(-6) M). It is suggested that the hypotensive effect of CK is mediated at least partly via Ca2+-dependent systems and inhibition of kininase II.
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PMID:[Mechanism of action of cyclokinins]. 631 9


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