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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An isometric tension measurement of ring segments was performed in the rabbit basilar and common carotid arteries in vitro to investigate the regional differences in the calcitonin gene-related peptide (CGRP)-induced vasodilation and the effect of subarachnoid hemorrhage on CGRP-induced vasodilation. CGRP elicited vasodilation of the rabbit basilar artery in a dose-dependent fashion when the artery was precontracted by 10(-5) M 5-hydroxytryptamine, whereas almost no relaxation occurred in the rabbit common carotid artery. The relaxation of the basilar artery was 64.03 +/- 1.85% at 3 x 10(-8) M CGRP, with an EC50 of 8.46 +/- 0.08. Two days after experimental subarachnoid hemorrhage, CGRP-induced relaxation of the rabbit basilar artery was 53.96 +/- 8.08% of the 10(-5) M 5-hydroxytryptamine-induced contraction, not significantly different from that of the basilar artery of the control rabbit. Our findings suggest that CGRP induces potent vasodilation in the rabbit basilar artery and that no impairment of vasodilation occurred after experimental subarachnoid hemorrhage. We speculate that CGRP may have therapeutic potential in cerebrovascular disease such as vasospasm after subarachnoid hemorrhage.
Stroke 1989 Jan
PMID:Effect of subarachnoid hemorrhage on calcitonin gene-related peptide-induced relaxation in rabbit basilar artery. 278 99

To elucidate the cardiovascular effects of alpha-human calcitonin gene-related peptide (CGRP), we infused CGRP intravenously at increasing rates of 3, 10, and 30 pmol.kg-1.min-1 during successive 15-min intervals into intact dogs, cardiac-denervated (CD) dogs, and cardiac-denervated dogs pretreated with beta-blockers. In intact dogs, the initial infusion rate of CGRP at 3 pmol.kg-1.min-1 did not produce significant hemodynamic changes, but the two higher infusion rates produced dose-dependent decreases in total peripheral resistance, mean arterial pressure, and left and right atrial pressures and produced dose-dependent increases in heart rate (HR) and cardiac output (CO). In addition, stroke volume decreased and pulmonary vascular resistance increased at the highest infusion rate. In CD dogs, CGRP produced qualitatively similar responses, although the increase in HR was markedly attenuated. The increase in CO was also attenuated, but the difference did not reach statistical significance. In CD dogs pretreated with beta-blockers, CGRP did not increase HR and the increase in CO was further attenuated. In a separate experiment, the lowest dose of CGRP (3 pmol.kg-1.min-1) was infused intravenously for 60 min in intact dogs; significant cardiovascular responses, qualitatively similar to those produced by higher rates of infusion, occurred. We conclude that CGRP is an extremely potent vasodilator and that the increase in HR is mediated primarily by autonomic reflexes.
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PMID:Cardiovascular effects of calcitonin gene-related peptide in conscious dogs. 280 93

The cardiovascular effects of calcitonin gene-related peptide (CGRP) were examined in conscious, unrestrained rats. Changes in mean arterial pressure, heart rate and cardiac output were continuously monitored before and after i.v. bolus injection of CGRP (0.1-5 micrograms/kg). Injection of the peptide caused dose-dependent reductions in mean arterial pressure (-24 +/- 4 mmHg), which were accompanied by marked tachycardia. Cardiac output was significantly increased after CGRP but little change was observed in stroke volume. CGRP also reduced total peripheral resistance (-46 +/- 6%). These data indicate that the hypotensive actions of CGRP are mediated through peripheral vasodilation rather than through reductions in cardiac output. Pretreatment with propranolol significantly reduced the tachycardia responses to CGRP from 81 +/- 11 beats/min to 36 +/- 4 beats/min, but did not abolish the increase in heart rate. These data suggest that CGRP produces a tachycardia through reflex increases in cardiac sympathetic tone and through possible direct positive chronotropic effects on the heart.
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PMID:Hemodynamic effects of calcitonin gene-related peptide in conscious rats. 350 66

Pheochromocytoma remains a clinical challenge to diagnose and manage. In addition, the association of multiple endocrine neoplasia syndromes with pheochromocytoma require the clinician's awareness to evaluate patients with pheochromocytoma (especially when bilateral) for abnormalities in thyroidal C-cell function with serum calcitonin determinations. The authors present a case of a 42-year-old woman initially diagnosed with, and treated for, cranial artery vasculitis because she had a stroke and a history of rheumatoid arthritis and asthma. Subsequent evaluation of episodic blood pressure increases, headache, and tachycardia revealed biochemical evidence of catecholamine overproduction. Bilateral adrenal masses were found on computed tomography scanning, and the functional nature of the adrenal masses was confirmed by a meta-Iodobenzylguanidine scan. Upon further evaluation, an elevated serum calcitonin concentration was demonstrated, which increased greatly with pentagastrin stimulation. C-cell hyperplasia was demonstrated by subsequent thyroidectomy, confirming the diagnosis of multiple endocrine neoplasia 2A. The difficulty in arriving at a correct diagnosis, the subsequent management, including bilateral adrenalectomy and thyroidectomy, and newer insight into the genetic abnormalities of multiple endocrine neoplasia 2A are discussed.
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PMID:Case report: bilateral adrenal pheochromocytoma. 804 54

The relaxant effects of calcitonin gene-related peptide (CGRP) on the 3rd branches of renal arteries obtained from stroke-prone spontaneously hypertensive rats (SHRSP), and Wistar-Kyoto rats (WKY) were investigated in vitro. CGRP elicited concentration-dependent relaxation, and the relaxant response was not affected by the mechanical removal of endothelium in either SHRSP or WKY. The CGRP-induced relaxant response was markedly greater in SHRSP than in WKY, whereas there was no significant difference in acetylcholine-induced relaxation, which was endothelium-dependent, between the two groups. Additionally, significantly enhanced reactivity to CGRP was also shown in spontaneously hypertensive rats compared to WKY; however, this reactivity was less than that observed in SHRSP. There were also no significant differences between WKY and SHRSP in the relaxation induced by forskolin, dibutyryl cyclic AMP, and 3-isobutyl-1-methylxanthine (IBMX). CGRP-induced relaxation was significantly potentiated in similar manner by the pretreatment with IBMX in both WKY and SHRSP. Incubation with glibenclamide (10(-6) M) had no effect on CGRP-induced relaxation in either group, the WKY or the SHRSP. These results suggest that CGRP produces endothelium-independent relaxation in the small renal arteries in the rat, and that the increased CGRP-induced relaxant response found in SHRSP may not be associated with the altered vasodilation mediated by cyclic AMP, or with functional changes in ATP-sensitive potassium channels.
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PMID:Relaxant effects of calcitonin gene-related peptide on isolated small renal arteries in stroke-prone spontaneously hypertensive rats. 804 80

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

Focal brain ischemia is the most common event leading to stroke in humans. To understand the molecular mechanisms associated with brain ischemia, we applied the technique of mRNA differential display and isolated a gene that encodes a recently discovered peptide, adrenomedullin (AM), which is a member of the calcitonin gene-related peptide (CGRP) family. Using the rat focal stroke model of middle cerebral artery occlusion (MCAO), we determined that AM mRNA expression was significantly increased in the ischemic cortex up to 17.4-fold at 3 h post-MCAO (P < 0.05) and 21.7-fold at 6 h post-MCAO (P < 0.05) and remained elevated for up to 15 days (9.6-fold increase; P < 0.05). Immunohistochemical studies localized AM to ischemic neuronal processes, and radioligand (125I-labeled CGRP) displacement revealed high-affinity (IC50 = 80.3 nmol) binding of AM to CGRP receptors in brain cortex. The cerebrovascular function of AM was studied using synthetic AM microinjected onto rat pial vessels using a cranial window or applied to canine basilar arteries in vitro. AM, applied abluminally, produced dose-dependent relaxation of preconstricted pial vessels (P < 0.05). Intracerebroventricular (but not systemic) AM administration at a high dose (8 nmol), prior to and after MCAO, increased the degree of focal ischemic injury (P < 0.05). The ischemia-induced expression of both AM mRNA and peptide in ischemic cortical neurons, the demonstration of the direct vasodilating effects of the peptide on cerebral vessels, and the ability of AM to exacerbate ischemic brain damage suggests that AM plays a significant role in focal ischemic brain injury.
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PMID:Discovery of adrenomedullin in rat ischemic cortex and evidence for its role in exacerbating focal brain ischemic damage. 852 87

Intensive training in a humid and warm environment can cause exertional heat stroke (ExHS) and rhabdomolysis (RBD) in military recruits. To investigate the role of vitamin D and monomeric calcitonin (CT) on the calcium metabolism in ExHS with RBD and acute renal failure (ARF), we studied 21 recruits with ExHS (mean age 21.4 years), 7 of which had ARF. Another 11 age-matched recruits with heat exhaustion (HE) and 11 healthy subjects were selected as controls. Our results showed that in 14 ExHS patients without ARF, mean serum creatinine (Cr) levels were significantly higher (151.16 vs. 106.08 mumol/l, p < 0.01), whereas serum osteocalcin (OC) levels were significantly lower (2.22 vs. 4.65 micrograms/l, p < 0.01) than in healthy controls. In 7 patients with ExHS and ARF, the mean serum Cr (774.38 vs. 105.20 mumol/l, p < 0.01), phosphorus (P) (2.26 vs. 1.26 mmol/l, p < 0.05), creatine phosphokinase (CPK) 274,143.97 vs. 85.78 IU/l, p < 0.05), intact parathyroid hormone (I-PTH) (299.81 vs. 18.66 ng/l, p < 0.05) and CT (13.58 vs. 6.63 ng/l, p < 0.01) levels on admission were significantly higher while the mean ionized calcium (iCa) levels were significantly lower than the healthy controls (0.9 vs. 1.18 mmol/l, p < 0.01). The mean serum 25-hydroxyvitamin D [25(OH)D] levels were not significantly different from healthy controls. However, mean serum 1,25-dihydroxyvitamin D [1,25(OH)2D] levels and the ratio of 1,25(OH)2D to 25(OH)D were significantly lower than healthy controls throughout the whole course of ARF. None of the 7 patients with ExHS and ARF developed hypercalcemia during the diuretic phase. Their mean serum I-PTH levels decreased significantly from 299 to 18 ng/l during the recovery phase (p < 0.05). Our study seems to suggest that the abnormal calcium metabolism in this unique patient group is in part caused by persistently decreased renal production of 1,25(OH)2D, although increased monomeric CT levels were associated with hypocalcemia. However, whether or not a causal relationship exists merits further investigation.
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PMID:A prospective study of calcium metabolism in exertional heat stroke with rhabdomyolysis and acute renal failure. 858 23

1. The relaxant responses to calcitonin gene-related peptide (CGRP) of the 3rd order branches of the superior mesenteric arteries (SMA) from 6 month old stroke-prone spontaneously hypertensive rats (SHRSP) and age-matched Wistar-Kyoto (WKY) rats were studied in vitro. 2. Cumulative addition of CGRP (10(-11)-10(-7) mol/L) caused endothelium-independent relaxation of arterial rings precontracted with noradrenaline (10(-6) mol/L). A markedly increased response to CGRP was observed in SHRSP. 3. There was no significant difference between SHRSP and WKY in relaxation produced by forskolin, dibutyryl cyclic AMP and 3-isobutyl-1-methylxanthine. 4. Pretreatment with glibenclamide (10(-6) mol/L) did not affect CGRP-induced relaxation in either SHRSP or WKY. 5. These results indicated that CGRP-induced vasodilation was increased in the small branches of SMA from SHRSP, and that this increase did not seem to be associated with an augmented response to cyclic AMP or with increased involvement of ATP-sensitive potassium channels.
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PMID:Calcitonin gene-related peptide-induced relaxation in isolated small superior mesenteric arteries from adult stroke-prone spontaneously hypertensive rats. 907 16

1. The effects of chronic NG-nitro-L-arginine (LNA) feeding on the endothelial function in isolated coronary arteries from stroke-prone spontaneously hypertensive rats (SHRSP) and normotensive Wistar-Kyoto (WKY) rats were studied. 2. A diet containing LNA (0.02%) was given to male SHRSP and WKY at 6 weeks of age and the coronary arteries were dissected on the 10th day of feeding. 3. In the SHRSP and WKY fed the LNA-free diet, acetylcholine (ACh) relaxed the precontracted ring segments of the coronary artery with intact endothelium in a dose-dependent manner. The reactivity was stronger in the WKY than in the SHRSP. However, the ACh-induced relaxation after the LNA-feeding was significantly stronger in the coronary arteries from the WKY than in those from the SHRSP. 4. The relaxation induced by the calcitonin gene-related peptide (CGRP) was endothelium-dependent and endothelium-independent. The degree of the response in the rats fed the LNA-containing diet was not significantly different from that in the rats fed the LNA-free diet. 5. The vasodilator response induced by sodium nitroprusside (SNP) was dose-dependent and similar in the rats fed the LNA containing diet and the LNA-free diet. 6. These findings indicate that chronic LNA feeding markedly impaired the endothelial nitric oxide formation in the coronary artery from young SHRSP.
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PMID:Changes of endothelial functions in the coronary artery after chronic nitroarginine feeding. 907 35


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