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

The morbidity and mortality due to cardiovascular complications of chronic arterial hypertension are distinctly reduced by persistent and successful antihypertensive therapy. The principal emphasis is on drug therapy. Diet and psychotherapy should be used as supportive measures. Examples of antihypertensive drugs available for general practice: saluretics, beta-receptor blockers, dihydralazine (Nepresol), alpha-methyldopa, clonidine (Catapresan), reserpine and guanethidine (Ismelin). With mild hypertension (diastolic blood pressure up to 105 mm Hq), monotherapy with a beta-receptor blocker or a saluretic is indicated first. Contrary to the medical rule never to use a combination preparation if it can possibly be avoided fixed combinations have proved valuable in hypertensive therapy and facilitate therapy for the hypertensive patient and for the doctor.
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PMID:[Therapy of hypertension in general practice. Comments on the recommendations of the German Antihypertension League (author's transl)]. 30 37

Ten patients with clinically complete cervical spinal cord transection of traumatic origin were studied. These subjects do not have supraspinal control of their sympathetic outflow and are prone to marked elevations of blood pressure during visceral and somatic stimulation. This is a result of reflex sympathetic activity via the isolated spinal cord. The arterial blood pressures and heart rates of these patients were recorded on separate occasions during elevation of the urinary bladder pressure and before and after treatment with propranolol, labetalol, phenoxybenzamine and guanethidine. Guanethidine seems to afford the best protection against the marked hypertension occurring during autonomic hyperreflexia. In contrast to the ganglionic blocking agents, it has no anticholinergic or CNS side-effects, and reflex sweating, a valuable indicator of an impending abdominal catastrophe, still occurs. The findings that negative inotropic drugs, i.e. propranolol, guanethidine and labetalol, reduce the marked elevations in pulse pressure which occur during acute bladder distension in quadriplegic patients, suggest that inotropic cardiac responses are mediated by cardiac sympathetic nerves which leave the spinal cord above the T5 level.
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PMID:Paroxysmal neurogenic hypertension and its prevention in patients with cervical spinal cord lesions. 48 97

Because of the multiplicity of disease conditions and diminished tolerance for drugs in the aged, it is necessary to know concomitant pathologic conditions to determine which antihypertensive drug to use. In the Philadelphia Geriatric Center, there are about 1,000 residents, between 70 and 100 years of age. About 40% have hypertension; almost 50% have or once had depression; there are many cases of hiatal hernia and/or peptic ulcer; in one subdivision of residents, almost 40% have renal disease with BUN above 30 mg/100 ml. In antihypertensive treatment, some individuals respond fairly well to reassurance and weight reduction, when obese, even without drugs. All are given a low-salt diet. A diuretic is first used--thiazide in cases of good renal function, furosemide with impaired renal function. Liquid potassium supplements are given. If there is but little reduction in blood pressure in several weeks, methyldopa is added in ascending doses, in cases with or without renal impairment. In hypertension with impaired renal function, furosemide and/or methyldopa were especially valuable. Furosemide as an antihypertensive drug was also noted to delay the onset of congestive heart failure. Since reserpine can aggravate peptic ulcer and can precipitate or aggravate depression, it should seldom be used to treat hypertension in the aged. Guanethidine is rarely used, since it can cause cerebrovascular insufficiency and marked weakness. High blood pressure should be reduced slowly in the aged, to avoid untoward effects.
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PMID:An approach to the treatment of hypertension in the aged. 105 27

A cardiogenic hypertensive chemoreflex was studied in 38 anesthetized and three unanesthetized dogs. Serotonin (100 mug/ml) injected into either the left atrium or small brancehes of the proximal left coronary artery produced a maximal response, with 96 +/- 18 mm Hg increment in mean aortic pressure within 6 +/- 2 seconds, lasting about 1 min; a later phase of the same hypertension lasted 9 +/- 5 minutes more and could partially be produced with serotonin injected into the thoracic aorta. Injections into the distal left coronary artery produced only the Bezold-Jarisch reflex. Concomitant with the immediate hypertension there were vagal and sympathetic efferent effects in both the sinus node and the atrioventricular (A-V) junction. Either of these effects could be selectively eliminated and the other augmented by direct local perfusion with an appropriate cholinergic (atropine 10 mug/ml) or adrenergic beta-receptor (propranolol 10 mug/ml) blocking agent. Bilateral vagotomy markedly attenuated but did not eliminate the acute hypertension, but it abolished both chronotropic and dromotropic effects. Phentolamine (2 mg/min i.v.) markedly diminished the hypertensive response. Guanethidine or reserpine pretreatment markedly diminished the hypertensive response; reserpine eliminated the electrophsiologic effects but guanethidine did not. Infiltration of serotonin around the main left coronary partially reproduced the reflex, but similar infiltration of xylocaine hydrochloride blocked the reflex. Serial section histologic studies of the region around the main left coronary atery in seven dog hearts and nine human hearts demonstrated the presence of a small structure resembling a chemoreceptor; its blood supply originated from the left coronary artery. Some possible clinical implications are discussed.
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PMID:Analysis of components in a cardiogenic hypertensive chemoreflex. 114 1

The influence of guanethidine on the nicotinic effects of acetylcholine was studied in anaesthetized atropinized dogs. Guanethidine (5 mg/kg i.v.) reversed the initial nicotinic pressor reaction, abolished the accompanying femoral vasoconstriction and reduced the increase of mean aortic flow. Therefore, nicotinic hypotension after guanethidine was due to a decrease of the peripheral vascular resistance. The height of the second pressor reaction was hardly affected by guanethidine. This drug inhibited the increases in mean aortic flow and heart rate but not the elevation of peripheral resistance, occurring at the secone nicotinic pressor phase. The present findings support the assumption that the initial hypertension is due to increased sympathetic outflow towards heart and vessels, whereas the second hypertension is due to adrenal medullary stimulation. The neurogenic femoral vasodilation at the onset of the second nicotinic pressor phase was blocked by guanethidine, which also inhibited the catecholamine-induced neurogenic vasodilation. These antagonisms may result from the interference of guanethidine with noradrenaline re-uptake.
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PMID:Influence of guanethidine on the nicotinic effects of acetylcholine in atropinized dogs. 115 45

To assess the role of the sympathetic nervous system in the development of genetic hypertension, blood pressure (BP) was recorded in conscious adult Lyon hypertensive (LH) and normotensive (LN) rats that had received daily injections of saline or guanethidine at 1-13 wk of age. Guanethidine abolished the pressor response to tyramine, decreased plasma norepinephrine by greater than 70% and plasma 3,4-dihydroxyphenylglycol by approximately 90%, and did not change plasma epinephrine. Bilateral adrenalectomy further reduced plasma norepinephrine to 8 and 5% of control levels in LH and LN rats, respectively. BP was lowered (-7%) in sympathectomized rats, but the mean absolute BP difference between LH and LN rats was unaltered. Despite marked supersensitivity to alpha-adrenoreceptor stimulation, phentolamine induced only a small transient depressor response, which was abolished by adrenalectomy in sympathectomized rats. It is concluded that the sympathetic nervous system is not necessary for the development of hypertension in LH rats. After sympathectomy, circulating catecholamines, which mostly derive from the adrenal medulla, play only a minor role in BP maintenance.
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PMID:Blood pressure maintenance in hypertensive sympathectomized rats. I. Adrenal medullary catecholamines. 168 45

The association between antihypertensive medications and depression has been recognised for over 40 years. More recently, our understanding of the role of neurotransmitters in the aetiology of depression has helped us understand how antihypertensive drugs cause depression. Biogenic amine depletion is now believed to underlie the organic nature of depression, and many of the drugs used to treat hypertension interfere with this system. There is now compelling evidence that both reserpine and alpha-methyldopa can induce or worsen depression through their actions on the central nervous system. beta-Blockers have also been implicated, but the data supporting the link between these drugs and depression are not as certain. Guanethidine, clonidine, hydralazine, and prazosin appear to pose little risk in causing depression, although rare occurrences have been reported. Diuretics, calcium channel blockers, and angiotensin converting enzyme (ACE) inhibitors appear to have the lowest association with depression and are therefore the drugs of choice when depression is a risk. Physicians should know which drugs introduce the risk of causing or worsening depression. The wide array of medications now available to treat hypertension offers alternatives that pose low risk. All patients receiving medication to treat hypertension should be evaluated periodically for depression, and if depression occurs, medication should be suspected as playing a role in its aetiology.
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PMID:Antihypertensive medications and depression. 207 96

Deoxycorticosterone acetate-induced hypertension in Yucatan miniature swine appears to involve elevated peripheral sympathetic activity. Abnormalities in renal function in these hypertensive animals are also apparent. To determine the extent to which renal nerve activity controls kidney function in animals with established deoxycorticosterone acetate hypertension, the effects of acute renal surgical denervation were assessed in five normal and 10 deoxycorticosterone acetate-treated swine. After 12 to 16 weeks of treatment, mean arterial pressure rose from the normal level of 110 to 120 to 164 +/- 4 mm Hg but was decreased to 131 +/- 4 mm Hg by anesthesia. In the normal animals, blood pressure under anesthesia was 114 +/- 9 mm Hg. Acute left kidney surgical denervation significantly decreased renal vascular resistance and increased renal blood flow, glomerular filtration rate, urine flow, and sodium excretion only in the treated animals. In an additional group of six normal and eight deoxycorticosterone acetate-treated swine, the responses to renal pharmacological denervation with intrarenal guanethidine were evaluated. Guanethidine had no significant effect on renal blood flow, vascular resistance, glomerular filtration rate, urine flow, or sodium excretion in the normal animals. In contrast, in the mineralocorticoid-hypertensive animals, guanethidine significantly decreased renal vascular resistance and caused a diuresis and natriuresis with no change in glomerular filtration rate. We conclude that, in deoxycorticosterone acetate-treated miniature swine with established hypertension, renal nerve activity appears to be elevated and important in determining renal hemodynamics and sodium and water excretion.
Hypertension 1986 Oct
PMID:Effects of acute renal denervation on kidney function in deoxycorticosterone acetate-hypertensive swine. 353 Oct 6

Guanethidine is a sympatholytic antihypertensive drug used for the treatment of severe or resistant hypertension. Previous clinical studies have documented the development of tolerance to guanethidine in humans and suggested that fluid retention or increased sensitivity of arterioles to endogenous catecholamines may be responsible for the tolerance development. In this study we investigated the role of the renin-angiotensin system in the development of tolerance to guanethidine in one-kidney, one-clip renovascular and spontaneously hypertensive rats (SHR) using the angiotensin-converting enzyme inhibitor captopril. In the one-kidney model, captopril (30 mg/(kg X day), orally) had no effect on the development of tolerance to guanethidine (50 mg/(kg X day), i.p.) when the drugs were coadministered for 2 wk. However, captopril enhanced the day 1 blood pressure-lowering effect and prevented the development of tolerance to guanethidine in male SHR. These results suggest that the renin-angiotensin system plays a major role in the development of tolerance to guanethidine in SHR but not in one-kidney, one-clip renal hypertensive rats. Thus, the etiology of the hypertensive state may dictate which physiological compensatory mechanisms are activated after antihypertensive drug administration.
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PMID:Effects of captopril on the development of tolerance to guanethidine. 632 27

We have previously shown that continuous captopril administration prevents hypertension from developing in the two-kidney, one-clip (2K, 1C) rat. The present investigation was designed to determine the mechanism(s) producing the hypertension. In one series of experiments captopril prevented pressure from increasing during an 8-wk treatment period. Relative to the last day of treatment, mean arterial pressure and total peripheral resistance (TPR) were increased and cardiac output was unchanged at 3, 7, and 28 days after captopril cessation. Plasma renin activity (PRA) was unchanged 3, 7, and 14 days after captopril cessation but was elevated at 28, 49, and 56 days after captopril cessation only in 2K, 1C rats with severe hypertension (systolic blood pressure greater than 180 mmHg). Guanethidine (45 mg/kg po, bid) did not prevent the development of 2K, 1C hypertension but did prevent the hypertension from developing after cessation of captopril. Blockade of the prostaglandin system with indomethacin (5 mg/kg + 50 micrograms X kg-1 X min-1) and of the kallikrein-kinin system with aprotinin (25,000 KIU + 150 KIU X kg-1 X min-1) for 2 h had no effect on captopril's antihypertensive effect. Additionally, no change in sodium or water balance was observed after captopril cessation. Taken together these data demonstrate that hypertension after captopril cessation is due to an increase in TPR. Additionally, the rise in TPR is due to both the sympathetic nervous and the renin-angiotensin systems since both systems must be functional before pressure rises.
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PMID:Hypertension after ending captopril administration: pathogenesis in 2-kidney, 1-clip rat. 639 Dec 6


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