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Query: UMLS:C0085580 (essential hypertension)
 14,686 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A role for calcium in human hypertensive disease has been suggested. However, the various, apparently contradictory, abnormalities of calcium metabolism observed in experimental and clinical hypertension do not allow for unambiguous description of the specific manner in which calcium contributes to the hypertensive process. We studied calcium metabolism in essential hypertension and used renin-sodium profiling, which reveals the biochemical heterogeneity of clinical hypertension. We observed renin-linked, heterogeneous deviations in circulating levels of the divalent cations, magnesium and ionized calcium, in addition to deviations in the calcium-regulating hormones, parathyroid hormone (PTH), calcitonin (CT), and 1,25 dihydroxyvitamin D (1,25 D). These renin-calcium metabolic deviations may both predict and contribute to the pathophysiology of salt-induced hypertension, the blood pressure effects of oral calcium supplementation, as well as the short and longer term effectiveness of calcium channel blockade. Altogether, these data suggest an intimate linkage between the hormonal control of calcium metabolism, the renin-angiotensin system and blood pressure regulation in human hypertension.
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PMID:The significance of calcium and calcium channel blockade in essential hypertension. 285 82

The renin-angiotensin-aldosterone system regulates blood pressure and volume homeostasis in addition to sodium and potassium metabolism, and may be linked to divalent cation metabolism as well as hypertensive disease. In essential hypertension, circulating serum magnesium and Ca++, and the calcium regulating hormones, parathyroid hormone, calcitonin and 1,25 dihydroxyvitamin (1,25D) are different in the various renin subgroups. Elevated blood pressure induced by such maneuvers as dietary salt loading is associated with exacerbations of these calcium metabolic deviations, and appears related to salt-induced changes in serum Ca++ or 1,25D levels. Short- or longer-term lowering of blood pressure with the calcium-channel blocker, nifedipine, or with calcium or magnesium supplementation is associated with a shift of renin system activity and calcium metabolic indexes back to average normotensive values in those subjects most susceptible to these hypotensive agents. These observations suggest that deviations in calcium metabolism in essential hypertension may be related to the pathophysiology of the hypertensive process. Further, renin system activity and calcium metabolic indexes such as serum Ca++ levels may help target specific subgroups of hypertensive populations most susceptible to various dietary or drug maneuvers, and thus may provide a basis to better understand and treat clinical hypertension.
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PMID:Renin, calcium metabolism and the pathophysiologic basis of antihypertensive therapy. 286 7

Insulin resistance occurs in a variety of conditions, including diabetes, obesity and essential hypertension, but its underlying molecular mechanisms are unclear. In type 2 (non-insulin-dependent) diabetes mellitus, it is insulin-resistance in skeletal muscle, the chief site of insulin-mediated glucose disposal in humans, that predominantly accounts for the low rates of glucose clearance from the blood, and hence for impaired glucose tolerance. Human type 2 diabetes is characterized by a decrease in non-oxidative glucose storage (muscle glycogen synthesis), and by the deposition of amyloid in the islets of Langerhans. Amylin is a 37-amino-acid peptide which is a major component of islet amyloid and has structural similarity to human calcitonin gene-related peptide-2 (CGRP-2; ref. 8). CGRP is a neuropeptide which may be involved in motor activity in skeletal muscle. We now report that human pancreatic amylin and rat CGRP-1 are potent inhibitors of both basal and insulin-stimulated rates of glycogen synthesis in stripped rat soleus muscle in vitro. These results may provide a basis for a new understanding of the molecular mechanisms that cause insulin resistance in skeletal muscle.
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PMID:Pancreatic amylin and calcitonin gene-related peptide cause resistance to insulin in skeletal muscle in vitro. 305 May 30

1. Spontaneously hypertensive rats (SHR) are useful for investigating the possible pathophysiological and neurochemical basis of human essential hypertension. 2. The accepted pathogenic mechanism of hypertension in SHR is an increased central sympathetic drive which results in an increased peripheral resistance. 3. The neurochemical basis of the increased sympathetic drive is unknown. The observation that there are reduced levels of neuropeptides (vasoactive intestinal peptide, neuropeptide Y, cholecystokinin octapeptide, neurotensin and calcitonin gene related peptide) in the spinal cord in SHR rats compared with age and gender matched Wistar-Kyoto normotensive rats could provide a basis for understanding the mechanism of hypertension in SHR.
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PMID:Altered levels of neuropeptides in the medulla and spinal cord of spontaneously hypertensive rats. 307 73

Total and ionized calcium, parathyroid hormone, calcitonin, and renin activity were measured in 27 untreated patients with essential hypertension. There was no relationship between any of these parameters and diastolic blood pressure. However, a significant inverse relationship was found between diastolic blood pressure and the ratio of either total or ionized calcium to parathyroid hormone (r = -0.40, P less than 0.05; and r = -0.38, P less than 0.05, respectively). The ratios did not correlate with patient age or plasma renin level. This preliminary finding suggests that the role of plasma calcium in hypertension may need to be analyzed in the context of overall calcium metabolism, as influenced by the parathyroid hormone. The role of an altered relationship between plasma calcium level and parathyroid hormone in the pathophysiology of essential hypertension remains to be studied.
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PMID:Parathyroid hormone and calcium. A relationship in hypertension. 341 13

Alterations of calcium metabolism in hypertensive disease have been increasingly observed, although the specific manner in which these alterations contribute to the increased blood pressure remains unclear. We have studied calcium metabolism in essential hypertension and have adopted an approach based on analysis of renin system activity, which emphasizes the heterogeneity of human hypertensive disease. With this approach we have defined parallel deviations of plasma renin activity, circulating ionized calcium, and calcium-regulating hormones, which suggest a calcium deficiency in some hypertensives and, an excess of calcium in others. These deviations can be used to predict and may mediate the blood pressure sensitivity of hypertensives to dietary salt, and may also target those individuals most likely to benefit from oral calcium supplementation. Calcium itself has enhanced antihypertensive effects in low renin subjects, having lower ionized calcium and higher endogenous 1,25-dihydroxyvitamin D values, and in subjects on higher dietary salt intakes. Calcium may alter pressure, at least in part, by suppressing endogenous vitamin D metabolites and by stimulating calcitonin secretion. We hypothesize that calcium-regulating hormones participate in the physiology of the renin-angiotensin system and in the pathophysiology of human hypertension.
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PMID:Alterations of dietary calcium intake as a therapeutic modality in essential hypertension. 353 Apr 9

Circulating levels of the calcium-regulating hormones, calcitonin, calcitriol, and parathyroid hormone, were analyzed in relation to plasma renin activity in 10 persons with normal blood pressure and in 51 persons with essential hypertension. Calcitriol (p less than 0.008) and parathyroid hormone (p less than 0.01) levels were elevated in hypertensives with low renin activity, whereas calcitonin levels were higher in patients with high renin activity (p less than 0.008), compared with normotensive controls and other hypertensive patients. Continuous relationships were observed between calcitriol levels and plasma renin activity in all patients (r = -0.65, p less than 0.001) and between parathyroid hormone levels and urinary sodium excretion in hypertensive patients with low renin activity (r = -0.63, p less than 0.01). Together, these results support a linkage between calcium metabolism and renin-sodium factors in essential hypertension. Calcium-regulating hormones and the renin-aldosterone system may coordinately mediate the blood pressure effects of differing dietary calcium and sodium intakes at the cellular level by altering cellular handling of monovalent and divalent ions.
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PMID:Calcium-regulating hormones in essential hypertension. Relation to plasma renin activity and sodium metabolism. 353 93

Alteration of calcium metabolism and changes in the levels of calcium-regulating hormones have been described in essential hypertension. In the majority of the reported clinical trials, calcium supplementation has resulted in a decrease in blood pressure. However, the mechanisms by which such a response would be mediated are entirely unknown. The present study confirmed that daily supplementation with 1.4 g of elemental calcium led to a significant decrease in both systolic and diastolic blood pressures (P < .01). Decrease in blood pressure was negatively correlated with increase in plasma calcitonin gene-related peptide (CGRP), measured with radioimmunoassay and by radioreceptor assay (P < .001), and positively correlated with decrease in intact parathyroid hormone (PHT) (P < .05). Following cessation of calcium supplementation, plasma CGRP levels and the blood pressure both reverted back to the base-line values, suggesting a direct effect of supplemented calcium on these two parameters.
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PMID:Antihypertensive effects of oral calcium supplementation may be mediated through the potent vasodilator CGRP. 813

Rat mesenteric resistance blood vessels are innervated by nonadrenergic, noncholinergic (NANC) vasodilator nerves. In vitro pharmacological, biological and immunohistochemical studies have provided evidence that the calcitonin gene related peptide (CGRP), a 37 amino acid peptide translated by the calcitonin gene, has a potent vasodilator effect and acts as a vasodilator neurotransmitter for NANC vasodilator nerves. The CGRP-containing vasodilator nerves inhibit adrenergic nerve-mediated vasoconstriction through direct relaxation of vascular smooth muscle, while adrenergic nerves suppress the neurotransmision of CGRP-containing nerves by inhibiting CGRP release from the nerve. Thus, CGRP-containing nerves and adrenergic nerves control vascular tone with reciprocal interferences. In in vivo studies, spinal cord (T9-12) stimulation of pitched rats produced a NANC depressor response mediated by endogenous CGRP, suggesting that CGRP-containing nerves are regulated by the central nervous system. The malfunction of CGRP-containing vasodilator nerves may be involved in cardiovascular diseases such as essential hypertension, coronal vasospasm, cerebral vasospasm and Renaud's phenomenon. It is suggested that the CGRP-containing vasodilator nerves play an important role in the regulation of vascular tone.
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PMID:[Calcitonin gene-related peptide and neural control of vascular tone]. 844 77

A total of 132 patients with stage I, II, essential hypertension were examined. Indices for central hemodynamics were determined as were the levels of parathormone, calcitonin, and ionized calcium. Radon baths in eukinetic and hypokinetic types of circulation caused a significant reduction in mean hemodynamic pressure and resulted in improvement of patency of arterioles. In so far as hyperkinetic type of hemodynamics is concerned, there was a significant reduction in cardiac index and an increase in specific peripheral resistance. The level of ionized calcium got increased in all the patients, the same being true of the levels of parathormone and calcitonin in cases of eukinetic and hyperkinetic types of circulation.
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PMID:[The effect of radon baths at the Khmel'nik health resort on the central hemodynamic indices and calcium-regulating hormones in patients with essential hypertension]. 863 Aug 22


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