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

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

This study examined whether vascular contractions related to the extracellular or intracellular pools of calcium activated by serotonin are altered by high arterial pressure in chronic hypertension. Coarctation hypertensive (CH), sham normotensive control (C), and one-kidney, one-clip hypertensive rats (1K1C) were used. Tail systolic, carotid, and femoral arterial pressures were measured. Thoracic aortas from 1K1C and CH rats, as well as abdominal aortas from 1K1C rats, but not abdominal aortas from CH rats were exposed chronically to elevated arterial pressure. Isolated rings of thoracic and abdominal aortas from all groups were suspended in muscle baths for isometric force recordings. After cellular calcium depletion, dose-response curves to extracellular calcium, in the presence of 10(-5) mol/L serotonin, were unchanged in thoracic or abdominal aortas among the three groups. In the presence of submaximum levels of serotonin (2 x 10(-6) mol/L), thoracic and abdominal rings without endothelium and abdominal rings with endothelium from the three groups showed similar responses to extracellular calcium. Such responses were significantly depressed in thoracic rings with endothelium from CH and 1K1C rats. Transient contractions attributable to release of an intracellular calcium pool by 10(-5) mol/L serotonin were enhanced significantly in hypertensive thoracic and abdominal aortas from 1K1C rats, when the pool was loaded with 0.25, 0.5, 1.0, 2.0, or 4.0 mmol/L CaCl2, as well as in hypertensive thoracic aortas from CH rats when the pool was loaded with 1.0, 2.0, or 4.0 mmol/L CaCl2, but not in normotensive abdominal aortas from CH rats at any calcium-loading concentration. Similar results were observed in aortas from C, CH, and 1K1C rats loaded with 1.0 or 2.0 mmol/L CaCl2 and stimulated with 2 x 10(-6) mol/L serotonin. Endothelial removal had no effect on these calcium-release contractions in abdominal aortas from any group, but enhanced contractions in thoracic aortas of 1K1C rats. In rings loaded with 2.0 mmol/L CaCl2, 2-nitro-4-carboxyphenyl-N,N-diphenylcarbamate inhibited contractions attributable to release of cellular calcium stores to a similar extent in C, CH, and 1K1C rats. This study suggests that serotonin-stimulated intracellular calcium-dependent aortic contractions are enhanced by elevated pressure in renal hypertensive rats.
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PMID:Effect of chronic high pressure on transient and tonic vascular contractions to serotonin in hypertension. 761 49

The possible complication of hypertension and epilepsy was investigated through the response in epileptic El mice. The systolic blood pressure in El mice (male, 8 weeks of age) and that in normal ddY mice (the parent strain of El mice) were compared by a tail-cuff method, using a programmed sphygmomanometer. The systolic blood pressure in El mice (120.5 +/- 5.6 mm Hg) was 28% (P < 0.01) higher than that in ddY mice (93.9 +/- 5.3 mm Hg). The higher systolic blood pressure in El mice was lowered by the acute intracerebroventricular administration of CaCl2 (10 mumol/kg, 30 min before measurement) or dopamine (30 nmol/mouse, 15 min before measurement), and was also improved by the chronic oral supplementation with 1.2% calcium (Ca2+) solution. Combining these results with those in our previous reports, where it is stated that lowering of Ca(2+)-calmodulin-dependent catecholamine synthesis increases the susceptibility to epileptic convulsions, we suggest that the increase in susceptibility to epileptic convulsion and occurrence of hypertension in El mice may be linked and that the two diseases may be associated.
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PMID:Hypertension in epileptic mice: a phenomenon related to reduction of Ca(2+)-dependent catecholamine synthesis in the brain. 766 12

1. The aim of the study was to characterize the functional beta 1-and beta 2-adrenoceptors of the rat left atrium and to investigate how these functional beta-adrenoceptor responses were altered in hypertension. The contractile responses of the left atrium from Wistar-Kyoto (WKY) and spontaneously hypertensive (SH) rats to isoprenaline, T-0509 and procaterol were characterized. Subsequently, the effects of selective beta 1-(bisoprolol) and beta 2 (ICI 118,551)-adrenoceptor antagonists were investigated on these responses. 2. The maximal combined contractile responses of the rat left atrium to cardiac stimulation and CaCl2, isoprenaline, T-0509 or procaterol were not altered by hypertension. 3. The sensitivities to CaCl2 (pD2 on WKY left atrium = 2.99), isoprenaline (8.82) and T-0509 (8.84) were not altered by hypertension. There was an increase in sensitivity to procaterol from a pD2 value of 7.21 to 7.61 in the left atrium of the SH rat. 4. The basal tension induced by cardiac stimulation alone was inhibited by bisoprolol at > or = 10(-8) M and by ICI 118,551 at > or = 10(-7) M and this inhibitory effect is probably due to membrane stabilizing activity. 5. The pKB values for bisoprolol against isoprenaline, T-0509 and procaterol on the WKY were 8.43, 8.68 and 8.18, respectively, and were not different from SH rat left atrium. 6. The pKB value for ICI 118,551 against isoprenaline was increased from 7.06 on the WKY to 7.44 on the SH rat left atrium. The pKB values for ICI 118,551 against T-0509 and procaterol on the WKY were 7.18 and 8.14, respectively and were not significantly different from the SH rat left atrium values. 7. These results suggest that: (a) procaterol stimulates the beta 1-, in addition to, the beta 2-adrenoceptors of the rat left atrium; (b) functional beta 1-adrenoceptors are not altered in hypertension, and (c) there is probably an increase in the affinity of procaterol and isoprenaline for the beta 2-adrenoceptors which underlies the small increase in the functional beta 2-adrenoceptor response in hypertension.
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PMID:Functional beta-adrenoceptors in the left atrium of normotensive and hypertensive rats. 787 75

To elucidate the antihypertensive mechanism of oral calcium supplementation in salt-dependent hypertension, we investigated the hypertensive activity of plasma from DOCA-salt hypertensive rats fed with (DS-Ca) or without (DS) a high calcium diet. Four weeks of calcium supplementation (4% CaCl2) attenuated the blood pressure increase in DS rats. Intravenous bolus injection of dialyzed plasma (1.0-kDa cutoff) from DS rats to normotensive rats resulted in a sustained elevation in blood pressure, whereas that from DS-Ca rats did not. As the endothelin concentration was not different between the two groups, the circulating hypertensive substance in DS rats may be identical to parathyroid hypertensive factor (PHF) and the inhibition of its expression by calcium may be involved in the hypotensive mechanism of high calcium diets in salt-dependent hypertension.
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PMID:Calcium supplementation inhibits the expression of parathyroid hypertensive factor in DOCA-salt hypertensive rats. 817 55

Recently, hypertension research has focused on altered cytosolic free Ca2+, [Ca2+]i, in cells of spontaneously hypertensive rats (SHR). In this work, a mechanism(s) responsible for regulating [Ca2+]i was studied with duodenal epithelial cells isolated from SHR and their control, normotensive Wistar-Kyoto rats (WKY). The equal specific activity of sucrase, an enzyme characteristic of microvilli, in both mucosal scrapings and isolated cells from SHR and WKY suggested that mucosal density of enterocytes was not largely different between the two strains. [Ca2+]i of the isolated cells was estimated with fura-2. Upon incubation in the presence of CaCl2, [Ca2+]i increased to a larger extent in SHR than in WKY cells. Ca2+ efflux based on measurements of [Ca2+]i was decreased in SHR cells. Correspondingly, it was found that 45Ca efflux at 10 sec was lower for SHR cells than for WKY cells. Specific activities of Ca(2+)-stimulated and Ca2+/calmodulin-stimulated ATPases in basolateral plasma membrane preparations were reduced in SHR cells. These results indicated that Ca2+ efflux was decreased by reduction in Ca(2+)-pumping ATPase activity in SHR enterocytes.
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PMID:Decreased calcium pump activity in duodenal epithelial cells from spontaneously hypertensive rats. 839 87

The metabolism of calcium and brain dopamine in spontaneously hypertensive rats (SHR) after the development of hypertension was investigated as a possible model for the hypertension mechanism. Serum calcium level in SHR was lower than that in the normotensive control. Wistar Kyoto rats (WKY, the parent strain of SHR). Conversely, bone calcification of SHR was higher than that in WKY. Possible mechanisms for the lower serum calcium level seen in SHR include a decrease in the availability of calcium from bone. The immunohistochemical dopamine levels in the neostriatum and nucleus accumbens in SHR were lower than those in WKY. In these regions, the dopamine level was increased by the intraventricular administration of CaCl2 through a central, calmodulin-dependent system. This study suggests, based upon previous pharmacological studies, that the decrease of the serum calcium level in SHR causes a decrease in central, calcium-calmodulin-dependent dopamine synthesis and a subsequent low level of dopamine in the brain that produces an increase in blood pressure through functions of cerebral dopaminergic neurons and peripheral sympathetic nerves. Our results suggest that this could be one of the mechanisms of hypertension in SHR.
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PMID:Decrease of central dopamine level in the adult spontaneously hypertensive rats related to the calcium metabolism disorder. 842 Jun 19

Reactivity of aortic and carotid strip from control; hypertensive; hypercholesterolemic; and hypertensive/hypercholesterolemic rabbits were studied. Maximal stress was less in strips from hypertensive/hypercholesterolemic animals. Norepinephrine sensitivity was increased in the carotid artery from hypertensive/hypercholesterolemic animals (EC50: 0.11 microM; 0.35 microM control). CaCl2 sensitivity during norepinephrine-induced contractions was enhanced by hypertension and hypercholesterolemia (carotid EC50: 0.10 mM; 0.38 mM control; aorta EC50: 0.12 mM; 0.82 mM control). Similar results were obtained during membrane depolarization. 5-hydroxytryptamine sensitivity (EC50: 0.15 microM carotid; 0.18 microM aorta) was decreased during hypertension (EC50: 0.51 microM carotid; 1.13 microM aorta) and by hypercholesterolemia (EC50: 1.76 microM carotid; 1.53 microM aorta). Our results support the hypothesis that hypertension and hypercholesterolemia increase vascular sensitivity by increasing Ca2+ permeability. Our results also suggest that hypertension and hypercholesterolemia selectively decrease 5-hydroxytryptamine-induced contractions.
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PMID:Effects of hypertension on hypercholesterolemia-induced changes in contraction of rabbit aorta and carotid artery. 883 Nov 4

Altered function of smooth muscle cell K+ channels have been reported in hypertension, but the contribution of various K+ channel types to these changes has not been completely determined. The purpose of this study was to compare the contribution of K+ channel types to whole cell K+ currents recorded from isolated thoracic aorta myocytes of 13 to 15 week old Wistar-Kyoto (WKY) and spontaneously hypertensive rats (SHR). Cells were isolated by collagenase and elastase digestion, and K+ currents recorded using whole cell voltage clamp methods at room temperature. Cells were superfused with a solution containing (in mmol/ L) 140 NaCl, 5 KCl, 2 CaCl2, 1 MgCl2, 10 HEPES, and 10 glucose. Pipettes were filled with a solution containing (in mmol/L) 120 KCl, 5 NaCl, 5 MgATP, 20 HEPES, and 10 BAPTA. The K+ currents (IK) recorded from a holding potential (HP) of -80 mV were smaller in the SHR compared to those in WKY (for example, at 20 mV: WKY = 6.1 +/- 0.6 pA/pF and SHR = 3.7 +/- 0.2 pA/pF). Values of cell capacitance were not different between the two groups (WKY = 25.2 +/- 3.2 pF and SHR = 26.6 +/- 1.9 pF). A component of IK inhibited by voltage (Kv) over the range from -80 to -20 mV was smaller in SHR. The voltage dependence of Kv availability and activation were not significantly different between the two groups. IK recorded from a HP = -20 mV (KCa) was not different between the two groups. Difference currents calculated from IK measured at HP of -80 and -20 mV (that is, Kv) were smaller in SHR as was the fraction of IK inhibited by 4-aminopyridine. These results suggest that under conditions of low intracellular [Ca2+] there are no differences in KCa currents, but the Kv currents are smaller in SHR. Inhibition of Kv by 4-aminopyridine (0.1 to 10 mmol/L) caused larger increases in basal tone in WKY aorta. These results suggest that Kv channels contribute to resting K+ conductance in both WKY and SHR aorta, but with a relatively larger contribution in the WKY.
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PMID:Comparison of K+ channel properties in freshly isolated myocytes from thoracic aorta of WKY and SHR. 887 45

This study examines the effect of long-term magnesium-deficient diet on blood pressure and vascular reactivity in aged spontaneously hypertensive rats (SHR) with established hypertension. Thirty-one-week old male SHR received control (0.15 per cent magnesium) and magnesium-deficient (0.015 per cent magnesium) diets for 30 weeks. Systolic blood pressure was measured by tail-cuff method. At the end of the study, the heart, aorta and kidney were collected to measure total magnesium and calcium concentrations; the ex vivo effects of the different magnesium diets on vascular reactivity were examined in isolated aorta and in the isolated perfused mesenteric vascular bed. After 30 weeks, magnesium deficiency had no effect on systolic blood pressure and heart rate of SHR. The tissue concentrations of total magnesium in aorta, heart and kidney were not modified by magnesium deficient diet. Total calcium concentration was significantly higher in the heart of the SHR fed the magnesium-deficient diet (p < 0.01). The aortic responsiveness to contractile agents norepinephrine, endothelin-1, CaCl2 and KCl, and to vasorelaxant agents acetylcholine and isoproterenol were not modified by magnesium deficiency. The vasoconstrictor activity to norepinephrine, CaCl2 and KCl was significantly enhanced in the isolated perfused mesenteric vascular bed of magnesium-deficient SHR (p < 0.05). In conclusion, magnesium deficient diet fails to elevate blood pressure in aged SHR maintained on deficiency for 30 weeks despite an enhanced ex vivo vasoconstrictor activity.
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PMID:Magnesium deficiency increases vasoconstrictor activity without affecting blood pressure of aged spontaneously hypertensive rats. 936 31


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