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)

The effect of calcium channel blockers on calcium homeostasis in postmenopausal osteoporotic women with arterial hypertension has not to date been defined. In the submitted study, the influence of nifedipine on serum parathyroid hormone (PTH), calcitonin and osteocalcin is followed in 11 patients. After one month of treatment, serum PTH markedly declined in all women and osteocalcin decreased in 10 patients. In contrast, serum calcitonin increased in five patients, whilst in another five the effect was just the opposite. In one woman this indicator was not affected. There are no mutual correlations between the mentioned indices. In conclusion, the calcitonin secretory process is not sensitive to calcium channel blockade within the present study. In spite of the fact that nifedipine inhibits PTH secretion in postmenopausal osteoporotic women, the direct effect of the drug on osteoblasts (not mediated by PTH) cannot be excluded.
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PMID:The effect of nifedipine on serum parathyroid hormone and calcitonin in postmenopausal women. 765 16

Dorsal root ganglia neuronal cell bodies synthesize the vasodilator neuropeptide calcitonin gene-related peptide and innervate the blood vessels and spinal cord sites (laminae I and II) involved in blood pressure regulation. We previously demonstrated that calcitonin gene-related peptide mRNA content is significantly decreased in dorsal root ganglia and that immunoreactive calcitonin gene-related peptide levels are reduced in laminae I and II of the dorsal horn of the spinal cord in the spontaneously hypertensive rat compared with Wistar-Kyoto control rats. To determine whether neuronal calcitonin gene-related peptide expression is also altered in mineralocorticoid-salt hypertension, we quantified calcitonin gene-related peptide mRNA levels in dorsal root ganglia and protein content in laminae I and II of the spinal cord in rats with mineralocorticoid-salt-induced hypertension. To control for pellet implantation, saline drinking water, and/or uninephrectomy, four normotensive groups were similarly studied. By Northern hybridization analysis, the ratio of calcitonin gene-related peptide mRNA to 18S rRNA was increased approximately fivefold in hypertensive rats (33 +/- 7) compared with each of the four normotensive control groups (average of the four groups, 6 +/- 0.5; P < .01, mineralocorticoid-salt group versus each group). The density of the peptide, quantified by computer-assisted image analysis, in laminae I and II in the hypertensive rats was also increased (66 +/- 1 versus average of the four groups, 46 +/- 2 arbitrary units; P < .001, mineralocorticoid-salt group versus each group). In conclusion, neuronal levels of calcitonin gene-related peptide mRNA and protein are increased in mineralocorticoid-salt hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1995 Jun
PMID:Enhanced neuronal expression of calcitonin gene-related peptide in mineralocorticoid-salt hypertension. 776 83

Current medical practice recommends the use of alternatives to estrogen-replacement therapy for the treatment of menopausal sequelae in younger women with breast cancer, although this clinical recommendation is undergoing reappraisal. Until prospective randomized studies addressing hormone use in this population are available, estrogen use in breast cancer patients will remain controversial. Because estrogen-replacement therapy is not the standard of practice and there is limited information available on nonestrogen therapies, women with breast cancer who are menopausal may not be prescribed or counseled about nonestrogen options. The efficacy, safety, and extent of use of most nonestrogen treatment modalities (other hormonal preparations, nonhormonal drugs, homeopathic preparations, and non-drug treatments) are not well documented and, unlike estrogen, many are selective in their benefit and do not share estrogen's universal impact. The use of several nonestrogen approaches for the prevention and treatment of osteoporosis has been promising. Traditional recommendations to maintain skeletal integrity, such as weight-bearing exercise; a diet rich in calcium and limited in caffeine, alcohol, and protein; avoidance of smoking; and measures to minimize trauma have been expanded to include the use or investigation of drugs (either alone or in combination). These drugs include progestins, vitamin D metabolites, injectable and intranasal synthetic salmon calcitonin, bisphosphonates, sodium fluoride, parathyroid hormone, growth factors, tamoxifen, etc. Strict control of the known risk factors, such as smoking, dyslipidemia, and hypertension as well as exercise, weight control, and the use of tamoxifen, are employed for the prevention and treatment of cardiovascular complications.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Nonhormonal alternatives for the management of early menopause in younger women with breast cancer. 799 60

Neuropeptides are ubiquitous in the sympathetic system and modulate transmission at the levels of the intermediolateral cell column, sympathetic ganglia, and neuroeffector junctions. Several neuropeptide-containing pathways from the hypothalamus and medulla modulate excitability of preganglionic neurons. Neuropeptides coexist with norepinephrine or acetylcholine in subpopulations of chemically coded, target-specific sympathetic ganglion neurons. Neuropeptide Y is colocalized in adrenergic vasoconstrictor neurons, whereas vasoactive intestinal polypeptide is colocalized in cholinergic sudomotor neurons. Neuropeptide expression is plastic; during development, neurons that switch from a noradrenergic to a cholinergic phenotype increase expression of vasoactive intestinal polypeptide, somatostatin, and substance P. Preganglionic inputs increase neuropeptide Y and inhibit substance P expression. Sympathetic denervation produces sprouting of sensory fibers containing substance P and calcitonin gene-related peptide in target tissues. Neuropeptides from preganglionic fibers (e.g., enkephalin) and primary afferents (e.g., substance P, vasoactive intestinal polypeptide) modulate transmission in sympathetic ganglia. Neuropeptide Y produces vasoconstriction, prejunctional inhibition of norepinephrine release, and postjunctional potentiation of norepinephrine effects. Plasma neuropeptide Y increases during intense sympathoexcitation, hypertension, and pheochromocytoma. Dystrophic neurites containing neuropeptide Y occur in human sympathetic ganglia during aging, diabetes, and dysautonomia. Sympathetic neuropeptides may thus have important clinical implications.
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PMID:Neuropeptides in the sympathetic system: presence, plasticity, modulation, and implications. 802 63

Glucocorticoids are highly valuable medication available to a physician, yet, their serious side effects have severely limited their use. Thus, the major purpose of our review is to provide a practical approach to increasing efficacy and minimizing side effects, that is increasing the benefit/risk ratio, of glucocorticoid therapy. The most effective way of avoiding their side effects, including infection, osteoporosis, atherosclerosis, is simply to avoid the overuse of glucocorticoids and to restrict their use to the truly indicated disease. Side effects can be reduced in part by the development of drug delivery systems, such as topical administration and targeting therapy. Combinations of calcium, vitamin D and sometimes thiazide or calcitonin, as compensatory therapy, have shown some favorable results for the prevention of osteoporosis. Although glucocorticoid therapy causes an increase of high-density lipoprotein and a decrease of lipoprotein (a) in serum, both are possibly preventive for atherosclerosis, hypertension and diabetes mellitus which are risk factors of atherosclerosis should be controlled. Future trends to remove their side effects will be obtained by more specific therapy based upon their pathogenesis.
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PMID:[Minimizing side effects of glucocorticoid therapy]. 816 80

Calcitonin gene-related peptide (CGRP), a 37 amino acid peptide resulting from the specific maturation processes of calcitonin gene products, was discovered in 1982. Its messenger RNA was isolated from a calcitonin cancer in rats similar to the human thyroid medullary carcinoma. CGRP is closely related to calcitonin and amylin, and to a lesser extent, to the region coding for the alpha chains of relaxins, insulin and insulin growth factors. In thyroid C cells, calcitonin itself is the major gene product, but CGRP is predominant in the central and peripheral nervous system. CGRP is found in most all tissues and is considered to be a neuromediator of particular importance in the cardiovascular system. CGRP is a powerful endogenous vasodilator in man; plasma concentrations of 56 pmol/l (slightly above physiological levels) provoke flush, hypotension and secondary catecholamine release and subsequent tachycardia. Intravenous injections lead to systemic vasodilatation and redistribution of blood flow to the skin, the brain, and probably the splanchnic territory. It has been suggested that CGRP plays a role in blood pressure modulation in certain pathological conditions. CGRP level is decreased in hypertension and increased in septic shock. In patients with terminal renal failure, CGRP is correlated with excess volaemia. It could affect blood pressure by redistributing blood flow, interacting with the renin-angiotensin system or by inhibiting aldosterone secretion. CGRP may also play a role in modulating cutaneous vascular constriction in Raynaud's syndrome and cerebral vascularization in patients with migraine or meningeal hemorrhage subsequent to rupture of cerebral aneurisms. CGRP increases arterial flow in the cavernous body. Coronarian vascular tone and cardiac performance (positive chronotrope and inotrope effects) are improved. CGRP has also been studied in connection with glucose metabolism and may have other endocrine effects. Finally, CGRP increases electrolyte and water flow in the colon and its bronchoconstrictor effect could be implicated in asthma. The clinical significance of plasma CGRP is not yet known although it may be a marker of poor prognosis in thyroid medullary cancer. Recent studies suggest that CGRP could be a useful therapeutic agent in severe Raynaud syndrome, impotency, ischaemic neurological lesions due to ruptured aneurisms and in severe heart failure.
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PMID:[Calcitonin gene-related peptide (CGRP)]. 817 60

The menopause is defined as cessation of menstruation, ending the fertile period. The hormonal changes are a decrease in progesterone level, followed by a marked decrease in estrogen production. Symptoms associated with these hormonal changes may advocate for hormonal replacement therapy. This review is based on the English-language literature on the effect of estrogen therapy and estrogen plus progestin therapy on postmenopausal women. The advantages of hormone replacement therapy are regulation of dysfunctional uterine bleeding, relief of hot flushes, and prevention of atrophic changes in the urogenital tract. Women at risk of osteoporosis will benefit from hormone replacement therapy. The treatment should start as soon after menopause as possible and it is possible that it should be maintained for life. The treatment may be supplemented with extra calcium intake, vitamin D, and maybe calcitonin. Physical activity should be promoted, and cigarette smoking reduced if possible. Women at risk of cardiovascular disease will also benefit from hormone replacement therapy. There is overwhelming evidence that hormone therapy will protect against both coronary heart disease and stroke, and there is no increased risk of venous thrombosis or hypertension. A disadvantage of hormone replacement therapy is an increased risk of forming gall-bladder stones and undergoing cholecystectomy. Unopposed estrogen therapy gives a higher incidence of endometrial cancer in women with an intact uterus, but the contribution of progestins for about 10 days every month excludes this risk. Breast cancer in relation to estrogen-progestogen therapy has been given much concern, and the problem is still not fully solved. If there is a risk, it is small, and only after prolonged use of estrogen (15-20 years). The decision whether or not to use hormone replacement therapy should, of course, be taken by the individual woman in question, but her decision should be based on the available scientific information. It is the opinion of the authors that the advantages of hormone replacement therapy far exceed the disadvantages. We suggest that every woman showing any signs of hormone deprivation should be treated with hormone replacement therapy. This includes women with subjective or objective vaso-motor symptoms, genito-urinary symptoms, women at risk of osteoporosis (fast bone losers), and women at risk of cardiovascular diseases.
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PMID:Postmenopausal hormone replacement therapy--clinical implications. 819 55

In anesthetized rats we examined whether calcitonin gene-related peptide activated renal pelvic sensory receptors and, if so, whether activation of renal pelvic calcitonin gene-related peptide receptors contributes to the inhibitory renorenal reflex response to renal mechanoreceptor stimulation. Calcitonin gene-related peptide (0.0026, 0.026, 0.26, and 2.6 mumol/L) administered into the renal pelvis increased ipsilateral afferent renal nerve activity in a concentration-dependent fashion (32 +/- 14%, 69 +/- 19%, 93 +/- 26%, and 253 +/- 48% [all P < .01], respectively). The increases in ipsilateral afferent renal nerve activity elicited by calcitonin gene-related peptide were associated with increases in contralateral urinary sodium excretion. The calcitonin gene-related peptide receptor antagonist human CGRP (h-CGRP) (8-37) (0.01, 0.1, 1.0, and 10 mumol/L) decreased the ipsilateral afferent renal nerve activity response to renal pelvic administration of calcitonin gene-related peptide (0.26 mumol/L) in a concentration-dependent fashion (29 +/- 4%, 33 +/- 12%, 76 +/- 9% [P < .01], and 86 +/- 13% [P < .01], respectively). In the presence of renal pelvic perfusion with vehicle, an increase in ureteral pressure of 5, 10, and 20 mm Hg increased ipsilateral afferent renal nerve activity by 13 +/- 7%, 41 +/- 7% (P < .01), and 95 +/- 15% (P < .01) and contralateral urinary sodium excretion by 8 +/- 1%, 24 +/- 4%, and 42 +/- 7% (all P < .05). The ipsilateral afferent renal nerve activity and contralateral natriuretic responses to graded increases in ureteral pressure (5 to 20 mm Hg) were unaltered by renal pelvic perfusion with h-CGRP (8-37) at 1.0 and 10 mumol/L.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1994 Jun
PMID:Renal sensory receptor activation by calcitonin gene-related peptide. 820 95

Estrogen deficiency is the main cause of postmenopausal osteoporosis. Replacement estrogen therapy protects the bone by reducing bone resorption and activating osteoblasts, as well as by promoting absorption of calcium and production of calcitonin. These preventive effects are especially marked in cancellous bone, provided estrogen therapy is initiated as soon as menstruation stops. Effects are dose-dependent and efficacy of the treatment is noticeable mainly during the period of administration. The rare contra-indications to estrogen therapy include hormone-dependent cancers, cholestatic jaundice, and large uterine myomas (for which surgical treatment is recommended). Metabolic disorders, arterial hypertension, and thyroid function disorders are less common with the new natural estrogens (estradiol) given orally or percutaneously to avoid hepatic passage of the drug. As for treatment induced cancers, sequential administration of a progestagen protects the endometrium and the relative risk seems negligible for breast cancer. Although concomitant use of a progestagen is mandatory, either natural progesterone or norpregnanes should be given to avoid adverse metabolic effects. Emphasis has recently been put on the role of concomitant progestagen therapy which may promote the formation of bone, probably by competing for glucocorticoid receptors in bone. There is still a need for prospective epidemiological studies, although evaluation methods and the long follow-ups needed raise significant problems.
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PMID:[Substitutive hormone therapy in postmenopausal osteoporosis. Are there any contraindications?]. 823 58

Isolation of calcitonin mRNA initiated studies on the multigene complex encoding a family of peptides: calcitonin, its terminal flanking peptides, calcitonin gene-related peptide (CGRP), and amylin. CGRP is expressed in alpha- and beta-forms that vary by one and three amino acids in rat and humans, respectively. Both alpha- and beta-CGRP are very similar in their biologic activities, therefore the role of duplicating the calcitonin/CGRP gene is unclear. CGRP behaves principally as a regulatory neuropeptide acting locally through interaction with target organ receptors that are either cyclic-AMP dependent, or capable of activating KATP channels of vascular smooth muscle. The dense distribution of CGRP-rich structures and the expression of mRNA in the central nervous system suggests that CGRP has a neuromodulator or neurotransmitter role not limited to vasoregulatory effects only, but like calcitonin, extends its action to physiologic, metabolic, and behavioral functions. Activation of perivascular sensory nerves stimulates the release of neuropeptides, including CGRP, which exerts a potent vasodilatory effect on venous and arterial vasculature. The increased levels of CGRP-like immunoreactivity were observed in volume overload states, in heart failure and myocardial infarction, and in some forms of hypertension. The beneficial effect of CGRP infusions was demonstrated in patients with congestive heart failure and also in subjects with neurological deficits after surgical treatment of subarachnoid hemorrhage. On the other hand, there are experimental studies on the inhibition of increased CGRP activity, in septic and shock conditions, in which the vascular hyperrelaxation could have deleterious effects.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Calcitonin gene-related peptide and regulation of human cardiovascular homeostasis. 839 Feb 69


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