Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The therapeutic efficacy of guanfacine was investigated in a group of 32 hypertensive patients. Guanfacine caused a marked decrease in total peripheral vascular resistance (by 19.8%, p less than 0.001) and, hence, in blood pressure (by 19.4%), p less than 0.001). A slight reduction in the heart rate (by 9.8%, p less than 0.01) was compensated by an increase in stroke volume (by 11.8%, p less than 0.05) so that cardiac output remained constant or was even slightly raised. After 4 weeks of treatment there was a regression of the left ventricular wall thickness and mass (by 7.43 +/- 2.44 g, p less than 0.05). Guanfacine monotherapy was effective in 75% of patients with moderate hypertension (using low doses 1-3 mg/day). In severe hypertensive disease a satisfactory therapeutic response was mostly achieved by a combination of Guanfacine (3-5 mg/day) with a beta-blocker, diuretic or vasodilator. Guanfacine is a promising agent in the long-term treatment of stable hypertension, particularly in patients, whom diuretics or beta-blockers are contraindicated.
 ...
PMID:[Hypotensive and hemodynamic effects of guanfacine in arterial hypertension]. 266 29

The hemodynamic effects of loud noise after central alpha 2-adrenoceptor stimulation were studied in 13 patients with mild (WHO 1) essential hypertension. The patients were randomized (double-blind) to treatment with either placebo or guanfacine 1-2 mg for four weeks and then crossed over and treated for another four weeks. All patients were exposed to a loud broad-band noise (105 dBA for 30 min) and all were studied both on placebo and guanfacine. Guanfacine significantly reduced the resting blood pressure from 141/92 to 134/88 mmHg (p less than 0.01) as well as heart rate at rest from 63 to 58 beats/min (p less than 0.05). Noise stimulation caused a significant increase in blood pressure and resistance in the placebo-treated group, while cardiac output decreased significantly. Pretreatment for one month with the central alpha 2-adrenoceptor stimulating agent guanfacine did not block the noise-induced pressor response nor the increase in peripheral resistance. A significant decrease in stroke volume was observed and cardiac output also tended to decrease in this group. It could be concluded that loud noise is a potent pressor stimulus which causes vasoconstriction and that the blood pressure response during noise could not be blocked by the centrally acting antihypertensive agent guanfacine. Since noise causes vasoconstriction it also induces an increased tone in the small arteries and, if the noise stimulus is sufficiently strong and repeated for a long time, it might cause structural changes in the resistance vessels and permanent arterial hypertension in humans.
 ...
PMID:Hemodynamic effects of loud noise before and after central sympathetic nervous stimulation. 288 13

The centrally acting alphamimetic antihypertensive drug, guanfacine, was studied in normotensive volunteers and patients with essential and renal hypertension. After acute (0.02 mg/kg, intravenously) and short-term (mean dose: 6.7 mg/day orally for 4 weeks) administration of guanfacine, systolic, diastolic and mean blood pressures (BPs), heart rate, cardiac output and right atrial pressure were measured by standard techniques. Cardiac index, stroke volume and total peripheral vascular resistance were calculated. After medium-term therapy (mean dose: 6 mg/day orally for 12 weeks), antihypertensive efficacy, as well as plasma renin activity and catecholamine levels, was determined. After intravenous administration, guanfacine lowered systolic, diastolic and mean arterial BPs after a brief and transient increase. Guanfacine exerted its antihypertensive action primarily by its effect on total peripheral resistance. Reflex tachycardia was not observed. Heart rate was reduced. Stroke volume increased and right atrial pressure decreased. These effects were maintained or enhanced during the 4 weeks of oral therapy that followed. In the 12-week study, significant reductions in systolic, diastolic and mean BPs were observed. With a constant dose of 3 mg/day for 1 week, BP decreased from 197/115/149 (systolic/diastolic/mean) to 166/97/126 mm Hg. After 4 weeks at varying doses, BP decreased to 157/91/118, and after 12 weeks, to 147/83/109. In the 12 patients treated for 4 weeks with 3 mg/day, a significant decrease from 192/111/145 to 151/87/114 mm Hg was observed, while in the 6 patients treated for 12 weeks with the 3 mg/day dose, the final readings showed a decrease of 50 mm Hg in systolic pressure, 30 mm Hg in diastolic pressure and 38.4 mm Hg in mean arterial pressure.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Hemodynamic and endocrine responses to guanfacine in normotensive volunteers and hypertensive patients. 351 26

The pharmacology of central alpha-adrenoceptor-stimulating agents is discussed, with particular reference to clonidine (Catapres; Boehringer Ingelheim) and guanfacine (Estulic; Sandoz), and their haemodynamic effects are compared and contrasted. The main differences between the effects of clonidine and guanfacine on hypertension are: guanfacine activates presynaptic alpha-adrenoceptors 10 times more selectively than clonidine; guanfacine has an alpha 2/alpha 1-selectivity ration 25 times higher than clonidine; clonidine decreases cardiac output and guanfacine decreases peripheral resistance, clonidine has no effect on stroke volume but guanfacine increases it; and when the clonidine withdrawal syndrome in the spontaneously hypertensive rat is compared with cessation of guanfacine treatment at an equipotent antihypertensive dose, the withdrawal syndrome after guanfacine appears later and is much less severe. Guanfacine may be preferable to clonidine as a central alpha-adrenoceptor stimulant in the treatment of hypertension.
 ...
PMID:Clonidine and guanfacine--comparison of their effects on haemodynamics in hypertension. 388 93

A chronobiological study of behavioral changes in Wistar Kyoto rats (WKY), spontaneously hypertensive rats (SHR) and stroke prone spontaneously hypertensive rats (SHRSP) was undertaken. Attention was focused on changes in ambulatory activity and drinking behavior using an Ambulo-Drinkometer, the effects of centrally acting antihypertensive drugs, and the relationship between behavioral changes and humoral factors. (1) The experiment was performed during a light-dark alternation cycle. Approximately 10 days were required for rats to acclimate to new cages. (2) Using power spectral analysis, a 24 hr periodicity was dominant in both sexes of WKY and SHRSP. A 120 hr periodicity was demonstrated in female SHRSP. This long periodicity may have been due to a female sexual rhythm. (3) Ambulatory activity of WKY and SHRSP tended to decrease with age. (4) After abrupt cessation of clonidine administration, an ambulatory ultradian rhythm was demonstrated. Guanfacine treated SHR showed less change in ambulatory ultradian rhythm than clonidine treated SHR. (5) Using a Drinkometer with attached metabolic cages, drinking counts, urinary volumes, urinary aldosterone and catecholamine excretion rates were higher during the dark phase than during the light phase. It was demonstrated that analysis of rhythmicities and measurement of behavioral amplitude are both needed in the study of behavioral pharmacology.
 ...
PMID:[A chronobiological study of behavioral changes in rats]. 674 14

The authors report here the case of a patient with severe deficits in arousal and sustained attention, associated with hemispatial neglect. These impairments were secondary to acute disseminated encephalomyelitis, with bilateral involvement of the medial nuclei and pulvinar of the thalamus. Treatment with the noradrenergic agonist guanfacine, previously used for attention deficits in attention deficit/hyperactivity disorder and stroke, was associated with a significant amelioration of both the spatial and sustained attention impairments in neglect. Guanfacine may prove to be a useful tool in the treatment of disorders of attention associated with neurological conditions.
 ...
PMID:Attention deficits following ADEM ameliorated by guanfacine. 2056 62