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)

Parathyroid hormone (PTH) is hypotensive in mammals and is a potent coronary vasodilator. Parathyroid hormone-related peptide (PTHrp) has been reported to have similar vascular activity. In the present study, the effects of human PTH (hPTH) and human PTHrp (hPTHrp) were compared in various in vivo and in vitro assays. In vivo studies included blood pressure measurement and coronary blood flow determination with labeled microspheres in anesthetized and cannulated normotensive rats. Isolated rat tail artery and portal vein helical strips were used in studying tension development in vitro. In the blood pressure assay, PTHrp was several times more potent than PTH. PTHrp was also significantly more potent than PTH in relaxing tail artery precontracted with arginine vasopressin (AVP). PTHrp and PTH both inhibited the spontaneously contracting portal vein, but again PTHrp was significantly more potent. PTHrp (1 microgram/kg) produced a greater increase in coronary blood flow as compared with the same dose of PTH. These data suggest that PTHrp is more potent than PTH in its cardiovascular actions. It is possible that PTHrp is the endogenous vasodilating ligand, and the structural similarity between PTH and PTHrp may explain the pharmacological action of PTH. It is therefore unlikely that PTH or PTHrp may be involved in the genesis or maintenance of hypertension. Because the parathyroid gland seems to be involved in some forms of essential hypertension, factor(s) other than PTH or PTHrp may be responsible.
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PMID:Cardiovascular effects of human parathyroid hormone and parathyroid hormone-related peptide. 751 45

Parathyroid hormone (PTH), a key hormone regulating plasma Ca level, is elevated in some essential hypertension, and conversly, hyperparathyroidism is associated with elevated blood pressure. However, such an effect would be paradoxical because PTH is a potent vasodilator. Parathyroid hormone-related peptide (PTHrP), which could act in a autocrine and paracrine manner in vascular smooth muscle cells and endothelial cells, would be a more potent vasodilator and could be produced in hypertensive vascular tissue. Calcitonin gene related peptide (CGRP), 37-amino acid neuropeptide results from alternative processing from calcitonin gene, is vasodilating peptide, and is localized in the central and peripheral nervous system involved in cardiovascular regulation. In some essential hypertensive patients, CGRP is reported to be at a low level.
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PMID:[PTH, PTHrP, and CGRP in hypertension research]. 928 6

Recent studies demonstrate low serum levels of 25-hydroxyvitamin D in patients with congestive heart failure (CHF). Although this may in part reflect reduced capacity for outdoor exercise, the possibility that poor vitamin D status increases risk for left ventricular hypertrophy (LVH), and its common sequel CHF, merits consideration. In cardiomyocytes, hormones which activate protein kinase C (PKC) -- including norepinephrine, angiotensin II, and endostatin, implicated in the pathogenesis of LVH -- induce a hypertrophic response analogous to that seen in LVH. Transgenic mice overexpressing PKC-beta2 or its upstream activator Galphaq in cardiac myofibers develop a syndrome similar to LVH. Parathyroid hormone (PTH) also activates Galphaq and PKC in cardiomyocytes, and provokes the expected hypertrophic response. Both primary and secondary hyperparathyroidism are associated with high risk for LVH. Moreover, in uncomplicated essential hypertension, left ventricular mass index has been shown to correlate very tightly with serum PTH levels, independent of blood pressure. This latter finding suggests that variations of PTH within the normal range can influence induction of LVH in at-risk subjects. If so, nutritional and lifestyle measures which modulate PTH secretion may have an impact on LVH risk. PTH secretion should be down-regulated by good vitamin D status -- achieved through supplementation or regular uv exposure -- and by vegan diets moderately low in bioavailable phosphate. Although high calcium intakes can likewise suppress PTH, they also boost renin secretion, which could have a countervailing effect on risk for LVH. Whether these nutritional measures do indeed influence LVH risk could be examined in prospective studies targeting patients at high risk, such as hypertensives.
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PMID:Nutritional modulation of parathyroid hormone secretion may influence risk for left ventricular hypertrophy. 1578 May 3

Parathyroid hormone has been related with the risk of hypertension, but the matter remains controversial. We examined the association of parathyroid hormone with central blood pressure and its determinants in 622 normotensive or never-treated hypertensive subjects aged 19-72 years without diabetes, cardiovascular or renal disease, or cardiovascular medications. The methods were whole-body impedance cardiography and analyses of pulse wave and heart rate variability. Cardiovascular function was examined in sex-specific tertiles of plasma parathyroid hormone (mean concentrations 3.0, 4.3 and 6.5 pmol/l, respectively) during head-up tilt. Explanatory factors for haemodynamics were further investigated using linear regression analyses. Mean age was 45.0 (SD 11.7) years, body mass index 26.8 (4.4) kg/m2, seated office blood pressure 141/90 (21/12) mmHg, and 309 subjects (49.7%) were male. Only five participants had elevated plasma parathyroid hormone and calcium concentrations. Highest tertile of parathyroid hormone presented with higher supine and upright aortic diastolic blood pressure (p<0.01) and augmentation index (p<0.01), and higher upright systemic vascular resistance (p<0.05) than the lowest tertile. The tertiles did not present with differences in pulse wave velocity, cardiac output, or measures of heart rate variability. In linear regression analyses, parathyroid hormone was an independent explanatory factor for aortic systolic (p=0.005) and diastolic (p=0.002) blood pressure, augmentation index (p=0.002), and systemic vascular resistance (p=0.031). To conclude, parathyroid hormone was directly related to central blood pressure, wave reflection, and systemic vascular resistance in subjects without cardiovascular comorbidities and medications. Thus, parathyroid hormone may play a role in the pathophysiology of primary hypertension.
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PMID:Parathyroid hormone may play a role in the pathophysiology of primary hypertension. 3328 96