Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085580 (essential hypertension)
 14,686 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To study limb vascular responses in man to elevations in plasma calcium concentrations, we infused test isosmolar solutions of CaCl2 (0.115, 0.230, and 0.460 meq calcium/min) and NaCl and control isosmolar solutions of NaCl into the brachial arteries of 10 normotensive men and eight men with essential hypertension of mild to moderate severity. Limb blood pressures were monitored, limb blood flow was measured by indicator-dilution, and limb vascular resistance was calculated as mm Hg/ml flow/min/100 cm3 limb volume. Measured concentration of calcium in limb venous plasma during infusion of 0.460 meq calcium/min was 11.5 +/- 0.8 meq/liter (mean +/- SEM) with individual values ranging up to 20 meq/liter. Changes in limb venous serum sodium, potassium, magnesium, and osmolality were similar during control and CaCl2 infusions. Decreases in limb venous blood hematocrit during CaCl2 infusions were the same or greater than those during control infusions. The infusions did not significantly change systemic blood calcium concentration or blood pressures. Limb blood flow decreased and resistance increased in response to CaCl2. Increments averaging as little as 2.2 meq/liter elevated limb resistance by about 45%. Log dose-response curves were linear. Responses did not differ in normotensives and hypertensives (P greater than 0.8). We conclude that the vascular response to acute elevation of plasma calcium concentrations up to 20 meq/liter in the limb oman is an impressive vasoconstriction. We found no evidence for abnormal vascular responses to calcium in essential hypertensive men.
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PMID:Similar vasoconstrictor responses to calcium in normotensive and esssential hypertensive men. 109 55

To clarify the mechanism of the antihypertensive effect of oral Ca loading, we studied the effect of Ca supplementation on salt-induced blood pressure elevations in patients with essential hypertension and DOCA-salt hypertensive rats. When the diet was changed from low to high salt (300 mEq/day), the percent increase in mean blood pressure was smaller (p less than 0.01) in the Ca-supplemented (2,160 mg/day) patients than in the Ca-restricted (250 mg/day) ones. Oral Ca loading resulted in a smaller weight gain, a greater urinary sodium excretion, and an increase in red cell Mg. In the experimental study, high Ca (4% CaCl2) intake attenuated the blood pressure elevation in DOCA-salt-treated rats, accompanied with an increase in urinary sodium excretion, with the resultant attenuation in intra- and extracellular sodium retention. The decrease in catecholamine contents of hearts was improved, and a higher survival rate was observed in Ca-supplemented DOCA-salt rats. The results suggest that Ca supplementation may prevent a rise in BP in salt-dependent hypertension by inducing natriuresis with the resultant attenuation in sodium retention. The altered intracellular Mg level in hypertensive patients and the normalization of enhanced sympathetic nervous activity in DOCA-salt rats may, in part, be involved in its mechanism.
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PMID:Calcium supplementation in salt-dependent hypertension. 195 52

Abnormalities of Ca2+ handling have been reported in patients with essential hypertension and in spontaneously hypertensive rats (SHR). In this study, responses of cytosolic Ca2+ to ADP in platelets of SHR were examined. Four- and seven-week-old male SHR and age- and sex-matched Wistar-Kyoto rats (WKY) were used. Basal levels of the intracellular Ca2+ concentration in platelets and responses to ADP were estimated using fluorescent indicator fura-2 in the medium containing 1 mmol/L CaCl2 and Ca2(+)-free buffer with 1 mmol/L EGTA. Basal levels of platelet cytosolic Ca2+ of SHR were significantly higher than those of WKY at 4 and 7 weeks of age in the presence of external Ca2+. However, no significant difference was observed in basal levels of platelet cytosolic Ca2+ in the Ca2(+)-free EGTA-containing buffer between SHR and WKY. The peak cytosolic Ca2+ concentration evoked by ADP was significantly diminished in SHR compared with WKY in the absence of external Ca2+, whereas the responses of platelet cytosolic Ca2+ to ADP were similar in SHR and WKY in the presence of external Ca2+. These results suggest that release from intracellular Ca2+ store is reduced in SHR and that the regulation of cytosolic Ca2+ in SHR is more dependent on extracellular Ca2+ compared with WKY.
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PMID:Responses of cytosolic free calcium to ADP in platelets of spontaneously hypertensive rats. 222 72

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.
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PMID:Electron spin resonance studies of erythrocytes from spontaneously hypertensive rats and humans with essential hypertension. 303 3

Using the fluorescent Ca-dependent dye quin-2 the authors measured the concentrations of free calcium in the platelet cytoplasm of rats with spontaneous hypertension (SHR) and in normotensive rats (NKWR) serving as control. There were no differences in the baseline levels of free Ca2+ between the platelets of the SHR and NKWR rats. When the cells were loaded with quin-2 in a calcium-free medium and transferred into a medium containing 1 mM of CaCl2, the concentration of Ca2+ in the platelets of the SHR rats became higher. An increase in the content of intracellular Ca2+ induced by thrombin administration was 70% higher in the platelets of the SHR rats as compared with the NKWR rats. The findings obtained suggest that the insufficiency of the Ca-transporting systems of the cellular membranes in primary hypertension described earlier is attended with disturbances in the regulation of the levels of cytoplasm free calcium.
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PMID:[Intracellular concentration of free calcium in thrombocytes: its characteristics in spontaneous hypertension]. 644 Oct 63