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

The effects of oral calcium loading on the development of hypertension were studied in spontaneously hypertensive rats (SHR). Forty-eight male SHR were divided into four groups according to treatment: control, calcium, deoxycorticosterone (DOC) and DOC + calcium. Both calcium groups received ad libitum 1.5% CaCl2 as drinking fluid. The DOC animals were injected with a mineralocorticoid, deoxycorticosterone trimethyl-acetate, 25 mg/kg, s.c., once a week. Systolic blood pressure (BP) was measured once a week by the tail cuff method. During the nine-week study, the development of hypertension was enhanced in the DOC group, while in the calcium group a blood pressure-lowering effect was observed when compared to the controls. Calcium also abolished the hypertensive effect of DOC. The maximal velocity of calcium transport was higher in "inside-out"-vesicles of red blood cells as compared to controls in both calcium-supplemented groups. DOC treatment resulted in elevated sodium and potassium contents in tail artery tissue, while the effect of the combination of DOC + calcium was equal to controls. On the other hand, the tissue Na:K ratio was decreased in both tail artery wall and heart in the calcium group. Calcium treatment diminished the excretion of phosphate in both groups, while the plasma phosphate concentration was lowered in the calcium group. In mesenteric arterial rings, DOC impaired nitroprusside-induced relaxation, while the relaxation was enhanced compared to control in both the calcium and DOC + calcium groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effect of high calcium intake on Ca2+ ATPase and the tissue Na:K ratio in spontaneously hypertensive rats. 153

To investigate the calcium dependence of salt-induced hypertension we concurrently measured blood pressure and serum ionized calcium in conscious normotensive female dogs undergoing five infusions: 1) sodium chloride (0.9%) 2) calcium chloride (10 mg/kg), 3) combined sodium chloride and calcium chloride, 4) nicardipine (1 micrograms/kg/min), and 5) combined sodium chloride and calcium chloride in the presence of nicardipine. While saline and calcium chloride infusions individually did not affect blood pressure, saline combined with calcium chloride significantly and consistently raised mean arterial pressure (MAP) (delta MAP = 7 +/- 2 mm Hg, P less than .001 v baseline). Serum ionized calcium (Caio) levels increased within the normal range with the infusion of calcium alone (1.32 +/- 0.03 to 1.48 +/- 0.01 mmol/L, P less than .005). Extracellular Caio rose less with the combined NaCl-CaCl2 infusion (delta Caio 0.10 +/- 0.01 v 0.16 +/- 0.02 mmol/L, P less than .02). The difference in calcium elevations could not be attributed to volume expansion alone, since saline infusion itself did not affect serum ionized calcium (1.32 +/- 0.3 to 1.31 +/- 0.01 mmol/L, P = NS). Furthermore, nicardipine prevented the pressor effect of the combined saline-calcium infusion. (delta MAP = -2 +/- 3 v 7 +/- 2 mm Hg, P less than .001), and restored the rise in extracellular Caio to that seen with the nonpressor calcium infusion (delta Caio 0.15 +/- 0.01 mmol/L v 0.16 +/- 0.02 mmol/L, P = NS). Altogether, these data demonstrate that the rise in blood pressure and ionized calcium following an acute infusion of sodium and calcium chloride are interdependent.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The pressor effect of sodium-volume expansion is calcium mediated. 166 68

1. The contractile responses of aortic ring preparations from Sprague-Dawley rats made hypertensive by 6-week dietary salt loading were studied. The test and control diet contained 8.0 and 0.3% NaCl, respectively. Aortic rings from salt-loaded rats showed enhanced sensitivity to noradrenaline (NA) but not to serotonin. Contractile responses to CaCl2 in Ca-free NA-containing medium was significantly enhanced in salt-loaded rats, but was unchanged in K(+)-depolarised medium. K(+)-induced relaxation (a functional indicator of Na-K adenosine triphosphatase activity) was sensitive to 10 mumol/L ouabain and was significantly attenuated in aortic rings from salt-loaded rats. The results suggest that hypertension induced by salt-loading is associated with enhanced sensitivity to NA, increased Ca2+ entry through receptor-operated channels, and impairment of Na-K ATPase enzyme activity.
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PMID:Altered responses of aortic smooth muscle from Sprague-Dawley rats with salt-induced hypertension. 166 59

Primary cultures of neonatal rat cardiocytes were exposed for 24 hours to culture media containing 0-2.0 mM extracellular calcium. Both atrial natriuretic factor (ANF) messenger RNA (mRNA) and ANF secretion were increased approximately threefold in the presence of 2.0 mM CaCl2 (vs. Ca2(+)-free medium). When cardiocytes were treated with the calcium channel blockers diltiazem, nifedipine, or verapamil, both ANF synthesis and secretion fell to 25-40% of control values. The choice of transcription start site on the ANF gene was not altered by the calcium channel blockers. When exogenous calcium was added to cardiocytes treated with verapamil, secretion of ANF was partially restored to control levels. High-performance liquid chromatographic analysis of medium from cardiocytes exposed to varying extracellular calcium concentrations or treated with calcium channel blockers for 24 hours revealed that the majority of secreted immunoreactivity (60-70%) migrated with pro-ANF (17 kDa) and that none of the various experimental manipulations significantly changed the ratio of pro-ANF to ANF in the media. These results were confirmed by immunoprecipitation analysis of the culture medium from the individual treatment groups. Treatment of cardiocytes for 24 hours with either the calcium ionophore A23187 or the phorbol ester 12-O-tetradecanoylphorbol 13-acetate increased ANF secretion. The combined use of these agents resulted in stimulation of both ANF secretion and ANF mRNA accumulation.
Hypertension 1990 Jan
PMID:Extracellular calcium regulates expression of the gene for atrial natriuretic factor. 168 46

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

Sustained smooth muscle contraction has been proposed to be regulated by either 1) sustained increases in intracellular Ca2+ concentration [(Ca2+]i)-dependent myosin phosphorylation or 2) diacylglycerol-dependent protein kinase C activation. We measured diacylglycerol mass with the diacylglycerol kinase assay and myoplasmic [Ca2+] with aequorin in swine carotid medial smooth muscle. Sustained and significant increases in [Ca2+], myosin light chain phosphorylation, and isometric stress were observed with histamine or endothelin stimulation. Neither stimuli, however, induced significant increases in diacylglycerol mass. Relaxation of histamine-stimulated tissues was induced by removal of histamine or removal of extracellular CaCl2 in the continued presence of histamine. The rate of decline of both [Ca2+] and force was similar in both protocols, suggesting that removal of Ca2+ (without removing the stimulus) was equivalent to removal of the stimulus. These data suggest that [Ca2+]i is the primary regulator of sustained swine arterial smooth muscle contraction, whereas diacylglycerol has, at most, only a minor role.
Hypertension 1990 Jun
PMID:[Ca2+], not diacylglycerol, is the primary regulator of sustained swine arterial smooth muscle contraction. 219 Sep 21

The effects of calcium and deoxycorticosterone (DOC) on blood pressure, plasma renin activity (PRA), urinary sodium excretion and aortic responses were studied in spontaneously hypertensive rats (SHR). The animals (age 9 weeks) were divided into four treatment groups: control, calcium, DOC and DOC+calcium (n = 12 and the mean systolic blood pressure 174-177 mmHg in each). Calcium was given as 1.5% CaCl2 in drinking fluid, and DOC trimethylacetate by weekly injections (25 mg/kg s.c.). During the 4-week study systolic blood pressure rose in all groups, but the increase was attenuated by calcium (final levels: control 201 +/- 3, calcium 186 +/- 3, DOC 206 +/- 2, DOC + calcium 203 +/- 2 mmHg, mean +/- SE). PRA was reduced in both groups receiving DOC, but it was not affected by calcium. Calcium supplementation increased urinary excretion of sodium in DOC-treated animals. DOC enhanced the in vitro contractility of helically cut aortic strips to noradrenaline, and decreased the relaxation of the strips to nitroprusside and nifedipine. The results indicate that calcium supplementation attenuates the development of hypertension in SHR, and that this attenuation is not mediated by the renin-angiotensin system. DOC abolished this lowering effect of calcium on blood pressure possibly by its action on vascular smooth muscle, resulting in increased vascular contractility and impaired relaxation.
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PMID:Effects of calcium and deoxycorticosterone on blood pressure, plasma renin activity and vascular reactivity in spontaneously hypertensive rats. 225 85

The effect of Bay K 8644, a dihydropyridine Ca2+ agonist, on in vitro contractile responses of inferior epigastric arteries from normotensive (N) and pre-eclamptic (P) subjects has been investigated, with a view to further defining the mechanism of the increased vascular sensitivity associated with pregnancy-induced hypertension. Bay K 8644 (10(-10)-10(-7) M) caused dose-dependent contractions of N as well as P arteries under resting conditions in the order: P greater than N and caused development of rhythmic contractions in both N and P arteries. Bay K 8644 effects were prevented by 3 X 10(-8) M Nifedipine (a Ca+2 antagonist). Bay K 8644 also significantly (P less than 0.05) enhanced the sensitivity as well as maximal contractile responses to CaCl2 in 40 mM K+-depolarized Ca-depleted N and P arteries in the order: P greater than N. The results suggest that the increased peripheral vascular sensitivity associated with pregnancy-induced hypertension may be due, at least in part, to enhanced activity of the potential-sensitive Ca2+ channels in arterial smooth muscle plasmalemma.
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PMID:Responses of arterial smooth muscle from normotensive and pre-eclamptic subjects to the calcium channel agonist, Bay K 8644. 245 Mar 90

The effect of calcium on plasma atrial natriuretic factor (ANF) concentration was determined in spontaneously hypertensive rats (SHR) and their control, Wistar-Kyoto (WKY) rats. CaCl2 10.5 mg (0.095 mmol) in 0.54 ml 5% glucose or an equal volume of vehicle alone was infused intravenously for 30 minutes into conscious precannulated SHR (vehicle, n = 16; CaCl2, n = 16) and WKY rats (vehicle, n = 25; CaCl2, n = 15). Direct systolic blood pressure was measured throughout the infusion period. Blood samples for serum total calcium and plasma ANF were obtained at the end of each experiment. The systolic blood pressure did not change significantly during infusion of the vehicle or CaCl2 in either strain. No significant difference was observed in serum total calcium concentration between SHR and WKY rats after vehicle (9.8 +/- 0.1 [mean +/- SEM] mg/dl vs. 10.0 +/- 0.1) or after CaCl2 infusion (12.2 +/- 0.3 vs. 12.2 +/- 0.2). Plasma ANF concentrations after both vehicle and CaCl2 infusion were significantly higher in SHR than in WKY rats (vehicle, 211 +/- 24 pg/ml vs. 129 +/- 11, p less than 0.05; CaCl2, 395 +/- 21 vs. 278 +/- 33, p less than 0.05). There were high degrees of correlation between serum total calcium and plasma ANF both in SHR (r = 0.77, p less than 0.001) and in WKY rats (r = 0.76, p less than 0.001). No significant difference was observed in the slopes of the regression lines of ANF as a function of the serum total calcium concentration between SHR and WKY rats.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1989 Jul
PMID:Calcium infusion increases plasma atrial natriuretic factor in spontaneously hypertensive rats. 252 28

LF 2.0254 is a new 1.4 dihydropyridine that relaxes vascular smooth muscles by blockade of calcium entry mediated by depolarisation. In rabbit aortas contracted by KCl (15 to 55 mM) or CaCl2 (2 mM), LF 2.0254 differs markedly from nifedipine and nicardipine because of its slow onset of action, the inhibitory effect increasing with the duration of tissular contact. LF 2.0254 has only slight negative chronotropic and inotropic effects on isolated guinea-pig atria as well as in anesthetized dogs after intravenous administration. Furthermore, in open-chest anesthetized dogs, LF 2.0254 decreases mean arterial blood pressure and since cardiac output is maintained total peripheral resistance is decreased. LF 2.0254 administered orally to perinephritic hypertensive dogs (0.1 and 0.3 mg/kg) and to spontaneously hypertensive rats (0.3 to 10 mg/kg) induces a more pronounced and long-lasting hypotensive action than nifedipine. In conclusion, these results suggest that LF 2.0254 could be useful in the treatment of hypertension associated or not with cardiac insufficiency.
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PMID:[Vasodilator effects of LF 2.0254, a new 1,4-dihydropyridine. Comparison with nifedipine]. 278 6


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