Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

According to immunohistochemical investigations kallikrein in the majors salivary glands is located predominantly at the apical border of the striated duct cells and as a luminal rim in the main excretory ducts. Comparatively the highest concentrations are observed in the submandibular gland of rats and cats in the cytoplasmic granules of the granular tubules. In normal humans and rats the kallikrein activity of parotid saliva is inversely related to flow rate and sodium concentration. An increased salivary kallikrein concentration is found in human essential hypertension and renoparenchymal hypertension associated with impaired kidney function. Furthermore in rats with various forms of hypertension (genetic hypertension, DOCTMA salt and renovascular hypertension) the salivary kallikrein secretion - as determined by the BAEE-esterase activity - is enhanced. In contrast to the kallikrein secretion the flow dependent sodium concentration of parotid saliva is reduced in human essential and renoparenchymal hypertension as well as in rats with various forms of experimental and genetic hypertension, which indicates an enhanced sodium reabsorption in the glandular duct system. Furthermore in most forms of hypertension, there is a tendency of higher potassium levels in the saliva. The pathogenesis of the enhanced glandular kallikrein secretion in hypertension is discussed with regard to a counterregulatory mechanism in hypertension as well as to a sympathicoadrenergic activation. The enhanced sodium reabsorption in the duct system in the various forms of hypertension could be the cause as well as a consequence of the enhanced kallikrein secretion.
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PMID:Salivary kallikrein excretion in hypertension. 39 78

The adrenaline content of specific brain stem areas was decreased in young (4 week-old) but not in adult (14 week-old) SHR. Some of these areas also showed increased PNMT activity, indicating a possible enhanced release or metabolism of adrenaline early in the development of the hypertension. Dopamine and noradrenaline levels, on the contrary, were not changed either in young or adult animals. Administration of a PNMT inhibitor to adult SHR resulted in a decrease of the blood pressure in SHR to control levels. These observations support the hypothesis of a participation of adrenergic mechanisms in the development of genetic hypertension, and indicate the possibility for the use of PNMT inhibitors as hypotensive agents.
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PMID:Adrenaline levels in brain stem nuclei and effects of a PNMT inhibitor on spontaneously hypertensive rats. 42 91

The microvasculature (MV) of serous membranes was compared in rats with spontaneous genetic hypertension (SHR) and in normotensive Wistar rats. The study showed that in hypertension MV lesions had a systemic distribution, as structural changes were present in every MV component (arterioles, precapillaries, capillaries, postcapillaries, venules, lymphatic capillaries, and postcapillaries, nerve fibers); these lesions were generalized, as similar alterations could be found in all serous membranes studied. A close resemblance observed between MV of serous membranes in SHR and in patients who died of hypertensive disease confirms the concept suggesting the existence of MV changes which were relatively specific for hypertension, along with those of the nonspecific nature. Specificity of the hypertensive process is manifested in severe vascular lesions of a peculiar type, while the nonspecific phenomena are represented by a combination of intravascular, perivascular, and minimal vascular alterations represented by a universal MV response to various stresses.
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PMID:[Microcirculatory bed of serous membranes in rats with spontaneous genetic hypertension]. 43 29

In two experimental models of established hypertension in the rat (two kidney, one clip renal and genetic hypertension), the maximum by which stroke volume and cardiac output could be increased during an acute preload stress was significantly reduced despite the concomitant development of left ventricular hypertrophy. Reversal of cardiac hypertrophy by prolonged treatment with methyldopa (range 3 to 6 weeks) during the established phase of spontaneous hypertension normalized arterial blood pressure and improved ventricular pumping ability. The improved performance was in part due to reduced impedance to ventricular ejection because it did not persist when peripheral resistance was increased by an acute administration of phenylephrine hydrochloride. Thus, hemodynamic as well as structural factors contribute to alterations in cardiac function during the chronic established phase of arterial hypertension.
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PMID:Cardiac pumping ability in rats with experimental renal and genetic hypertension. 49 96

The occurrence of main coronary risk factors was assessed in the families of 211 men under age 56 from East Finland. Fifty men were survivors of a recent myocardial infarction, 55 had died of myocardial infarction, 53 suffered from uncomplicated angina, and 53 were healthy reference men. Familial hyperlipidaemia was twice and familial hypertension three times as common in case as in reference families; other risk factors were equally common in both. Familial hypercholesterolaemia was commonest in the families of men with fatal myocardial infarction, and multiple type familial hyperlipidaemia in those of men with angina. Any increase in familial aggregation of coronary heart disease was invariably paralleled by increased aggregation of hyperlipidaemia and hypertension, with the most impressive aggregation of both traits in case families with a maternal history of early coronary death. It is concluded that most of the familial aggregation of coronary heart disease is mediated by familial aggregations of hyperlipidaemia and hypertension.
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PMID:Aggregation of coronary risk factors in families of men with fatal and non-fatal coronary heart disease. 50 67

The effect of increased dietary calcium on the development of hypertension in spontaneously hypertensive (SH) rats was investigated by feeding lab chow fortified with calcium carbonate (2.5% calcium, hCa) beginning at 4 wk of age. A control SH group was fed regular lab chow (1.2% calcium, rCa). Two groups of age-matched Wistar-Kyoto (WKY) rats were treated in parallel. Systolic blood pressure (BP) was measured weekly until the age of 18 wk using a tail cuff method. The hCa diet significantly attenuated the time course of hypertension in SH rats even though both SH groups eventually developed hypertension. The hCa also lowered BP in WKYs, but to a lesser extent. Urine output (24-hr volumes) was not affected by hCa, but in both SH and WKY groups fed the hCa diet, the excretion of Na+, K+ and Ca++ was markedly elevated at 11, 15, and 19 wk of age. Urine osmolality was also elevated. Plasma Na+, Ca++ and osmolality were not significantly altered by the diet in either SH or WKY rats; plasma potassium was significantly lower in the SH group fed the hCa diet than in the group given rCa. The hCa diet did not significantly affect the body or heart, kidney, adrenal, or thymus weights. The results suggest that hCa diet may attenuate genetic hypertension by inducing an osmotic diuresis.
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PMID:Increased dietary calcium lowers blood pressure in the spontaneously hypertensive rat. 51 84

Changes in systolic blood pressure (SBP), heart rate (HR), heart rate and plasma renin concentration (PRC) have been compared in three different groups of rats between the ages of 5 and 20 weeks. The groups were: spontaneously hypertensive rats (SHRs), atenolol-treated SHRs (200 mg/kg/day orally throughout the 15 weeks) and normotensive rats of the same strain (WKYs). Treatment with atenolol markedly inhibited the onset of genetic hypertension, reduced HR and PRC from the outset and diminished the heart weight/body weight ratio. Comparison of changes in these parameters in atenolol-treated SHRs, control SHRs and WKYs strongly suggests that the mechanism of atenolol's preventive action against hypertension development in SHRs primarily involves its effects on heart and on the renin--angiotensin system.
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PMID:Chronic atenolol treatment and hypertension development in spontaneously hypertensive rats. 63 Nov 88

Several models of experimental hypertension are described (neurogenic, mineralocorticoid, renovascular and genetic hypertension). An activation of the sympathetic nervous system is seen in these situations (increases in sympathetic nervous discharge, in the synthesis of noradrenaline and in the level of plasma catecholamines). This activation may be connected with biochemical abnormalities within the medulla which have been noticed for catecholamines and serotonin. These medullary abnormalities could themselves depend on abnormalities situated at higher levels (hypothalamus). The factors which determine the central problem and their mechanism of action are still hypothetical (e.g. the direct effect of sodium on the brain, the effect of stress and the environment as well as genetically determined biochemical abnormalities of the central nervous system). In the case of essential hypertension in man, available data are limited to the levels of plasma catecholamines which suggest an increased sympathetic activity of central origin when these levels are elevated.
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PMID:[Arterial hypertension: the role of the central nervous system. II. Experimental and clinical study (author's transl)]. 64 71

Genetically hypertensive (GH) rats of the New Zealand strain and normotensive (N) rats were sympathectomized from birth with 6-hydroxydopamine (100 mg/kg,s.c, on alternate days, seven treatments). In adult treated rats from each strain (GHTr and NTr), blood pressure was lower than normal. Functional tests and electron microscopy showed that denervation was virtually complete in mesenteric and hindlimb arteries; the innervation of the renal artery was little affected. Ganglionic blockade still caused a large fall in blood pressure in treated rats. Vascular resistance was higher in blood-perfused hindlimbs and tails of GH rats than in those of N rats; in contrast, resistance was similar in limbs and tails of GHTr and NTr rats and was greater than that found in untreated N rats. Saline-perfused limb vessels had neither neurogenic nor myogenic tone and resistance was higher in GH limbs (whether these were from treated rats or not) than in untreated N limbs. In saline-perfused NTr limbs, there was a paradoxical structural adaptation (probably luminal narrowing) of the hindlimb blood vessels and resistance was higher than in untreated N rats. The resistance of saline-perfused GH and GHTr limbs was similar. A high peripheral resistance appears to be the main mechanism sustaining genetic hypertension, and the integrity of the vasomotor sympathetic nerves is necessary for the development of this form of experimental hypertension.
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PMID:Blood pressure and vascular resistance in genetically hypertensive rats treated at birth with 6-hydroxydopamine. 66 60

The presence of three pools of exchangeable calcium (A,B and C) was demonstrated by the method of investigating the kinetics of 45Ca efflux from the fat issue of rats; the two most slowly exchangeable pools (B and C) reflected the distribution of intracellular calcium. The calcium content in the pools B and C of the fat tissue of rats with spontaneous hypertension was increased by 71 and 29%, respectively, as compared to that in the normotensive controls. Adrenalectomy leads to a marked redistribution of intracellular calcium, but the differences between spontaneously hypertensive rats and normotensive rats in the calcium content in the pools B and C are nonetheless maintained. These differences in the distribution of intracellular calcium may be the direct cause of the change in the hormonal sensitivity of the adipocytes of rats with spontaneous genetic hypertension.
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PMID:[Disturbance of the intracellular calcium distribution in the fatty tissue of rats with spontaneous genetic hypertension]. 73 88


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