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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Rats housed individually in glass metabolism cages develop hypertension. Since previous experiments have provided some evidence for the involvement of the sympathetic nervous system in the maintenance of the hypertension, the present work was designed to explore the possible involvement of the sympathetic nervous system in the genesis of isolation-induced hypertension. Male and female Wistar rats were treated neonatally with guanethidine, with a protocol designed to produce an extensive peripheral sympathectomy; control rats received saline. The effects of isolation on systolic blood pressure and fluid and electrolyte balances were studied when the rats were mature. Guanethidine-treated rats did not develop hypertension in response to isolation whereas control rats did. There were no significant differences between the fluid and electrolyte balances of the guanethidine-treated rats compared with controls throughout the period of isolation. It is concluded that a fully functional sympathetic nervous system is required for the development of isolation-induced hypertension, but its involvement is not through a modulation of renal function.
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PMID:The influence of neonatal treatment with guanethidine on the development of isolation-induced hypertension in adult rats. 661 95

Conscious normotensive and two-kidney, one clip Goldblatt hypertensive dogs were studied to determine the influence of the sympathetic and renin-angiotensin systems on the blood pressure and renal blood flow. Renal blood flow was monitored in a single kidney of the normotensive dogs and in the contralateral kidney of the hypertensive dogs. Saralasin was infused intravenously (i.v.) at 1 microgram/kg/min for 15 minutes in untreated and guanethidine-treated animals. Guanethidine (i.v.) decreased blood pressure (BP) in the hypertensives at X = 16 days after Goldblatt clamp application, but not in the normotensives, and did not affect renal blood flow or vascular resistance in either group. Saralasin produced approximately the same BP decrease in both untreated and guanethidine-treated hypertensives at X = 12 days after Goldblatt clamp application; the combined effect of the drugs was greater than saralasin alone. Blood flow and vascular resistance of the hypertensives' contralateral kidney were not significantly affected by saralasin in these experiments. No sustained effect on BP or renal blood flow was obtained with saralasin in the normotensives. Administration of furosemide was utilized to increase plasma renin activity (PRA) in another series of experiments. In both normotensives and hypertensives, PRA was elevated at 2-3 hours after furosemide application, being greater in the hypertensives. When the renin-angiotensin system was activated in this manner, saralasin had a significant hypotensive and renal vasodilator effect in the hypertensives, but not in the normotensives.
Hypertension
PMID:Sympathetic and renin-angiotensin system influence on blood pressure and renal blood flow of two-kidney, one clip Goldblatt hypertensive dog. 698 57

1. The antihypertensive effect and side-effects of the new centrally acting agent guanfacine (BS 100-141, Estulic) and guanethidine (Ismelin) were compared in a single-blind, cross-over study. The study consisted of two active treatment periods of 6 weeks each, both preceded by a 1-3 weeks placebo period. 2. Sixteen ambulant patients (six male, ten female) with mild or moderate hypertension were admitted to the study. The patients were also receiving diuretic therapy (clopamide 10-20 mg daily). On average the optimal daily dose of guanfacine was 3 mg and of guanethidine 20 mg. 3. An equally large and significant decrease in blood pressure was produced by both drugs. Both guanfacine and guanethidine caused a very slight reduction in heart rate. Mild orthostatic hypotension occurred in 11 patients during guanethidine therapy. Dryness of the mouth occurred in 13 patients taking guanfacine.
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PMID:Comparative study of two antihypertensive agents: guanfacine and guanethidine. 699 86

Autonomic dysreflexic hypertension occurs in up to 80% of spinal cord injury patients with lesions thoracic level 6 or higher. Pharmacologic agents directed at each part of the autonomic dysreflexic circuit were tested for efficacy in a rat model. Guanethidine (15 mg/kg intraperitoneally), alpha-methyl-paratyrosine (20 mg/kg intraperitonally), propranolol (3 mg/kg intraperitonally) and control were each tested on groups of three rats with intrinsic control blood pressure measurements. Results show an increase of 15 +/- 5 mm Hg diastolic pressure in control animals compared with no detectable increase with guanethidine or alpha-methyl-paratyrosine. There was an 11 +/- 2 mm Hg increase in diastolic pressure with propranolol. In conclusion, screening drug trials show that the ganglionic blocking agent, guanethidine, and competitive tyrosine uptake precursor, alpha-methyl-paratyrosine, effectively blocked dysreflexic hypertension, whereas the beta-blocker, propranolol, did not.
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PMID:Pharmacologic treatment of autonomic dysreflexia in the rat. 791 19

Effective therapy (Rx) in primary hypertension (PH) for 50 years, has featured sympathetic nervous system (SNS) mechanisms. Ganglionic blockers and reserpine were pre-eminent in the 1940s (mydriasis, ileus, impotence, peptic ulcer). Guanethidine, and in the 1960s clonidine and methyldopa, were step II agents to thiazide Rx in the 1950s. Reserpine depletes brain (depression) and peripheral (PPH) noradrenaline (NA) storage sites, guanethidine depleted NA storage via blockade of reuptake. Venomotor sympathoplegia resulted in postural hypertension. An analogue, metaiodobenzyguandine is used in diagnosis and Rx of pheochromocytoma. Clonidine lowers both central and PPH neuronal NA release via both stimulation of alpha agonist adrenoreceptors (sedation) and specific imadazoline binding sites (IBS). Methyldopa lowers pressure via PPH induced NA release (retrograde ejaculation) and via alphamethyl NA on central alpha-2 receptors (depression). The alpha-2 and alpha-2 receptor antagonists (alphaRA) cause reflex tachycardia and first-dose hypotension. Recently a two-fold incidence of congestive heart failure after alphaRA in treated primary hypertensives question their role in PH. The beta RA, with or absent alphaRA, remain premier since the 1970s due to mortality benefit in systolic dysfunction and post myocardial infarction, certifying the role of the SNS in the pathogenesis and sequelae and Rx of PH. The future includes beta RA, specific IBS agents, angiotensin (AII) RA with avid presynaptic AII affinity and vasopeptidase inhibitiors that raise peptides and suppress SNS.
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PMID:Sympatholytic therapy in primary hypertension: a user friendly role for the future. 1198 8

The treatment of essential hypertension still consists of the judicious combination of two or more agents. The chemical nature, pharmacology, side effects and relative merits of two groups of drugs are reviewed: (1) agents interfering with the synthesis, storage and release of endogenous catecholamines and (2) oral diuretic agents. Rauwolfia compounds, bretylium tosylate, guanethidine, alpha-methyldopa and pargyline hydrochloride comprise the first group; thiazide derivatives, phthalimidine compounds and spironolactones constitute the second. Guanethidine is the most potent and most extensively used agent in the second group. While not yet fully assessed, alpha-methyldopa and pargyline hydrochloride are useful in selected cases. The intrinsic hypotensive properties of oral diuretics, their low incidence of side effects and their ability to potentiate the more potent agents make them useful adjuncts in the long-term treatment of hypertension. Attention is drawn to the potential diabetogenic and hyperuricemic effects of the thiazides and phthalimidine compounds.
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PMID:NEWER DRUGS IN THE TREATMENT OF HYPERTENSION. 1428 40

The aim of the present study was to evaluate the effect of short-term adrenergic blockade on the rate of whole-body protein turnover and leucine oxidation, and on protein synthesis in specific tissues in male rats. Adrenergic blockade was induced by guanethidine (100 mg/kg body weight subcutaneously). The control group was treated with saline. On the second day, the parameters of whole-body protein and leucine metabolism were evaluated using a primed constant intravenous infusion of L-[1-(14)C]leucine. Protein synthesis in tissues was determined on the basis of L-[1-(14)C]leucine incorporation. Guanethidine treatment caused a decrease in norepinephrine in skeletal muscle. Whole-body leucine oxidation and leucine oxidized fraction were higher in guanethidine-treated rats. There was an insignificant effect of guanethidine on whole-body proteolysis, protein synthesis and leucine clearance. However, protein balance was negative due to the larger difference between protein synthesis and proteolysis in guanethidine-treated animals compared to controls. In guanethidine-treated rats, protein synthesis was higher in the gastrocnemius muscle and in the kidneys and lower in liver and spleen. Changes in the small intestine and colon were insignificant. In addition, a marked decrease in concentration of several amino acids has been observed in the liver, the kidneys and the spleen. It is concluded that adrenergic blockade induced by guanethidine is associated with significant changes in protein metabolism, leucine oxidation and amino acid concentrations in several tissues. The most important consequences of treatment are considered to be a negative effect on protein balance, increased protein turnover in skeletal muscle and kidneys and decreased protein synthesis in the liver and spleen. These changes may also be induced by administration of other sympathetic blocking agents, e.g. in treatment of hypertension.
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PMID:Protein metabolism in guanethidine-treated rats. 1537 58


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