Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.23.15 (renin)
 35,795 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of guancydine (1-cyano-3-tert-amylguanidine) on systemic and renal hemodynamics was studied in nine patients with arterial hypertension. Antihypertensive drugs were withheld for 15 days before beginning the investigation. Average sodium intake was 105 meq/24 hours in some patients and 25 meq/24 hours in others. Patients received placebo during a control period that averaged 14 days. Guancydine was given for 7 to 18 days at an average dose of 21 mg/kg of body weight. Although mean arterial blood pressure decreased significantly in all patients, it reached normal levels in only two. There was no change in cardiac output. Glomerular filtration rate and renal plasma flow remained unchanged, whereas urinary sodium excretion diminished, suggesting an activation of the renin-angiotensin-aldosterone system. A substantial gain in body weight was noted. Nausea, vomiting, constipation, somnolence, restlessness, mental confusion, asthenia, and urine retention were observed. The anti-angiotensin effect of guancydine that has been described in animals was not observed.
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PMID:Effect of guancydine on systemic and renal hemodynamics in arterial hypertension. 32 1

Calcium-entry blocking agents resemble established dilators such as diazoxide, minoxidil and hydralazine in that they act predominantly on the arterial resistance vessels and have little or no effect upon the veins. They have therefore been evaluated in the treatment of hypertension. Controlled studies have shown that verapamil and nifedipine are effective in decreasing blood pressure when given as sole agents. The antihypertensive effect of nifedipine is additive with that of a beta blocker, and nifedipine is also effective when given as a "third step" agent in combination with a beta blocker (or alpha methyldopa) and a diuretic. In contrast to other directly acting dilators, nifedipine causes, at most, only moderate stimulation of renin secretion and verapamil does not increase renin release at all; neither drug induces sodium retention. Both verapamil and nifedipine produce a moderate incidence of unwanted effects; these are mostly subjective in nature, but verapamil may cause constipation that is occasionally severe and nifedipine sometimes causes ankle swelling. Calcium-entry blockers should be considered as initial therapy when some contraindication exists to the use of other standard drugs. Nifedipine appears preferable to hydralazine for use in combination with a beta blocker and a diuretic: it is at least as effective as hydralazine and has a lower incidence of serious adverse effects.
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PMID:Calcium-entry blocking agents in the treatment of systemic hypertension. 285 16

The major antihypertensive mechanism of calcium antagonists is by decreasing the systemic vascular resistance, modified by the counter-regulatory responses of the baroreflexes and the renin-angiotensin-aldosterone system. In severe hypertension, the concept that calcium overload of the vascular myocyte could precipitate or aggravate peripheral vasoconstriction provides a logical basis for the use of these agents as first choice therapy; nifedipine, especially, has been well tested. As monotherapy for mild to moderate hypertension each of the three first-generation agents compares well with beta-blockers. Calcium antagonists may have a special role in the therapy of certain patient groups (elderly, black) or in those subjects whose life style involves intense physical or mental exertion (hemodynamics better maintained than with beta-blockade) or in patients with early end-organ damage such as left ventricular hypertrophy or renal insufficiency. However, the goal blood pressure may not be reached during monotherapy so that drug combinations may be required. Further indications for these compounds are as follows. Verapamil and diltiazem are frequently used in supraventricular tachycardias including acute and chronic atrial fibrillation. In the arrhythmias of the Wolff-Parkinson-White syndrome, there is the potential danger of provocation of anterograde conduction. Further indications for calcium antagonists, still under evaluation, include congestive heart failure (controversial), hypertrophic cardiomyopathy (verapamil), primary pulmonary hypertension (high doses required), Raynaud's phenomenon (nifedipine and diltiazem effective), peripheral vascular disease (proof not yet documented), cerebral insufficiency and subarachnoid hemorrhage (nimodipine promising), migraine, exertional bronchospasm, renal disease, atherosclerosis (experimental), and primary aldosteronism (nifedipine inhibits aldosterone release). Second-generation agents include dihydropyridines, such as nitrendipine, nicardipine, felodipine, amlodipine, nisoldipine, nimodipine, and isradipine. From these will be selected agents that are longer acting and provide higher vascular selectivity. New preparations of existing agents include slow-release formulations of nifedipine, verapamil, and diltiazem. Minor side effects include those caused by vasodilation (flushing and headaches), constipation (verapamil), and ankle edema. Serious side effects are rare and result from improper use of these agents, as when intravenous verapamil is given to patients with sinus or atrioventricular nodal depression from drugs or disease, or nifedipine to patients with aortic stenosis. The potential of a marked negative inotropic effect is usually offset by afterload reduction, especially in the case of nifedipine. Yet caution is required when calcium antagonists, especially verapamil, are given to patients with myocardial failure unless caused by hypertensive heart disease. Drug interactions of calcium antagonists occur with other cardiovascular agents such as alpha-adrenergic blockers, beta-adrenergic blockers, digoxin, quinidine, and disopyramide.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Calcium channel antagonists. Part III: Use and comparative efficacy in hypertension and supraventricular arrhythmias. Minor indications. 315 29

A case of pseudo-Bartter's syndrome associated with hypokalemic myopathy was presented. A 37-year-old housewife was admitted to our hospital because of muscle cramps with muscle weakness and tetany. There was a history of facial edema and constipation, which have been managed with "Kanpo medicine (Chinese medicine)" and laxatives for several years. The patient was amenorrhea 3 months before entry. She began to experience muscle weakness and muscle cramps associated with gait disturbance 2 or 3 months before admission. On physical examination, she was thin with positive Trousseau's and Chvostek's signs. Laboratory studies revealed hypokalemia, low urinary excretion of potassium, hypocalcemia, metabolic alkalosis, elevated creatine phosphokinase (CPK), increased levels of plasma renin activity and plasma aldosterone concentration, and decreased sensitivity to pressor effect of angiotensin II. Potassium supplementation resulted in restoration of her symptoms and normalization of low serum calcium and elevated CPK levels. She was diagnosed to be pseudo-Bartter's syndrome due to anorexia nervosa. The mechanism(s) of hypokalemia in our case was discussed.
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PMID:[A case of pseudo-Bartter's syndrome associated with hypokalemic myopathy]. 322 Jan 55

Many studies have confirmed that the treatment of mild and moderate hypertension reduces mortality and morbidity from cardiovascular accidents and cardiac and renal failure; more recent studies suggest that there is some beneficial effect on ischemic heart disease. The harmful metabolic effects of some hypotensive agents on serum potassium, magnesium, uric acid, glucose, renin and lipids might reduce the beneficial effect of controlling raised blood pressure. Also, the adverse effects associated with most antihypertensive drugs have decreased quality of life and, possibly, compliance in many patients. In assessing the value of newer antihypertensive agents, other effects of the drugs must be taken into account. The calcium-channel antagonist verapamil produces a dose-dependent reduction in blood pressure with little postural effect. There is little change in heart rate and the major antihypertensive effect results from a decrease in peripheral vascular resistance, with no accompanying increase in cardiac output. In 75 patients followed for more than 1 year, tolerance to verapamil did not appear to develop, nor were there any significant changes in serum electrolytes or creatinine clearance. Fasting serum lipid levels were measured in 15 patients before and after 3 months of treatment with verapamil (80 to 160 mg, 3 times a day); there was no change in cholesterol, triglycerides or high-density lipoproteins. Verapamil is, therefore, an effective hypotensive agent with a rapid onset of action. Tolerance does not develop with prolonged use, nor does it appear to affect electrolytes or serum lipids adversely. Constipation appears to be its only limiting adverse effect.
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PMID:Long-term results with verapamil in essential hypertension and its influence on serum lipids. 351 14

The antihypertensive efficacy of monotherapy with the calcium antagonists nifedipine (n = 60) and verapamil (n = 43) was investigated in patients with essential hypertension. Relationships between age, pretreatment blood pressure, pretreatment plasma renin activity, and hypotensive response were examined. Intraindividual differences in the responses to both drugs were also studied (n = 16). Treatment with verapamil had to be discontinued because of constipation in one patient; treatment with nifedipine was discontinued because of headache in 11 and ankle edema in one. The antihypertensive efficacy of nifedipine and verapamil was comparable and was positively related to pretreatment mean blood pressure (p less than 0.001) and inversely to pretreatment plasma renin activity (p less than 0.05). With verapamil, the fall in blood pressure correlated positively with the patient's age (p less than 0.001). Thus, calcium antagonists can be used as first-line drugs, especially in older and low renin patients. The relationship between the antihypertensive response and pretreatment blood pressure suggests that there may be a calcium influx-dependent vasoconstrictor mechanism in essential hypertension which may be more pronounced in patients with low plasma renin.
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PMID:Factors influencing the hypotensive effects of calcium antagonists. 634 78

The centrally-acting antihypertensive drug guanfacine was studied in a group of 11 moderate hypertensives. In doses of 2 mg daily, an average reduction in diastolic blood pressure of 10.8 mmHg was achieved. Side-effects were few when doses were maintained below 3 mg daily. The blood pressure reduction was associated with a fall in plasma renin activity and an average weight gain of 1.8 kg. When guanfacine was tried in 6 very severe hypertensives who had proved resistant to other antihypertensive drugs, a similar reduction in diastolic pressure of 7 mmHg was achieved using a dose of 3 mg daily. It is considered that guanfacine is a useful new antihypertensive drug, effective in mild hypertension, and side-effects are few if doses are maintained below 3 mg daily. Above this dose, side-effects became prominent, and these included sedation, dry mouth and constipation.
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PMID:Guanfacine: a new centrally-acting antihypertensive agent. 701 31

We report the case of a 72-year-old female with pure autonomic failure, a rare entity, whose diagnosis of autonomic dysfunction was determined with a series of complementary tests. For approximately 2 years, the patient has been experiencing dizziness and a tendency to fall, a significant weight loss, generalized weakness, dysphagia, intestinal constipation, blurred vision, dry mouth, and changes in her voice. She underwent clinical assessment and laboratory tests (biochemical tests, chest X-ray, digestive endoscopy, colonoscopy, chest computed tomography, abdomen and pelvis computed tomography, abdominal ultrasound, and ambulatory blood pressure monitoring). Measurements of catecholamine and plasmatic renin activity were performed at rest and after physical exercise. Finally the patient underwent physiological and pharmacological autonomic tests that better diagnosed dysautonomia.
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PMID:Hormonal and cardiovascular reflex assessment in a female patient with pure autonomic failure. 1101 9

Nocturnal urinary continence is dependent on 3 factors: 1) nocturnal urine production, 2) nocturnal bladder function and 3) sleep and arousal mechanisms. Any child will suffer from nocturnal enuresis if more urine is produced than can be contained in the bladder or if the detrusor is hyperactive, provided that he or she is not awakened by the imminent bladder contraction. Urine production is regulated by fluid intake and several interrelated renal, hormonal and neural factors, foremost of which are vasopressin, renin, angiotensin and the sympathetic nervous system. Detrusor function is governed by the autonomic nervous system which under ideal conditions is under central nervous control. Arousal from sleep is dependent on the reticular activating system, a diffuse neural network that translates sensory input into arousal stimuli via brain stem noradrenergic neurons. Disturbances in nocturnal urine production, bladder function and arousal mechanisms have all been firmly implicated as pathogenetic factors in nocturnal enuresis. The group of enuretic children are, however, pathogenetically heterogeneous, and two main types can be discerned: 1) Diuresis-dependent enuresis - these children void because of excessive nocturnal urine production and impaired arousal mechanisms. 2) Detrusor-dependent enuresis - these children void because of nocturnal detrusor hyperactivity and impaired arousal mechanisms. The main clinical difference between the two groups is that desmopressin is usually effective in the former but not in the latter. There are two first-line therapies in nocturnal enuresis: the enuresis alarm and desmopressin medication. Promising second-line treatments include anticholinergic drugs, urotherapy and treatment of occult constipation.
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PMID:Enuresis--background and treatment. 1119 46

Gitelman's variant of Bartter's syndrome, inherited hypokalemic alkalosis, is caused by mutation in the thiazide-sensitive NaCl co-transporter (NCCT). The main clinical symptoms are: muscular weakness, carpopedal spasm, constipation and short stature. The diagnosis was suspected in five children according to clinical criteria. All patients exhibited carpopedal spasm during febrile illness, three patients had short stature. Biochemical features were: metabolic alkalosis, hypokalemia, hypomagnesemia, low IGF-I levels, hyperkaliuria, hypernatriuria, hypocalciuria and normoprostaglandinuria. Three patients had elevated plasma renin activity and hyperaldosteronism. Mutational analysis of the NCCT gene confirmed the diagnosis in all five patients. Different forms of therapy, potassium and magnesium substitution, spironolactone and indomethacin failed to fully correct hypokalemia and hypomagnesemia, but markedly improved growth velocity and normalized IGF-I levels in the three patients with short stature. During therapy, clinical symptoms disappeared. We conclude that Gitelman's syndrome is a disorder with a variable symptom profile, but can be suspected on clinical signs already in early childhood. The early diagnosis is essential in preventing complications.
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PMID:Clinical, biochemical and molecular genetic data in five children with Gitelman's syndrome. 1145 84


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