Effects of clonidine and guanfacine in essential hypertension

Abstract

Daily doses of 0.3 mg clonidine and 3 mg guanfacine were equiactive in decreasing blood pressure and heart rate in 17 subjects with essential hypertension. Clonidine decreased cardiac output and guanfacine decreased total peripheral resistance, while clonidine had no effect on stroke volume but guanfacine increased it. Both clonidine and guanfacine decreased plasma renin activity. Naloxone, 0.4 mg iv, reversed the antihypertensive effect of clonidine but was ineffective even at higher doses (1.6 mg iv) when subjects were treated with placebo or guanfacine. It is suggested that the hemodynamic differences between the two centrally acting alpha 2-adrenoceptor agonist antihypertensive drugs may at least in part result from the involvement of opioid mechanisms only in the action of clonidine.

Captopril and opiate antagonism in essential hypertension.

“…(b) It is possible that longterm captopril leads to higher opioid levels than could be antagonised by this dose of naloxone. (c) It is possible though unlikely that the interaction is limited to a subgroup of patients, as had been reported with clonidine (Farsang et al, 1984). (d) Concomitant diuretic therapy which was required for adequate longterm blood pressure control may have had a confounding effect.…”

Enteral Guanfacine to Treat Severe Anxiety and Agitation Complicating Critical Care After Cardiac Surgery

“…12 Ultimately, however, we chose guanfacine because EIRG appears to be associated with a better hemodynamic profile (less hypotension and increased cardiac output), improved psychometric performance and neurologic function, decreased negative effect on EEG (electroencephalography) sleep patterns, and less potential for withdrawal symptoms after discontinuation than does clonidine. [13][14][15][16][17] While existing data demonstrate a theoretical benefit of EIRG over clonidine, these studies are more than 30 years old and were conducted in the outpatient setting. We believe more contemporary and targeted studies in ICU patient populations are, therefore, warranted.…”

Central Sympatholytic Drugs

“…Reduction in heart rate, rather than stroke volume, is mainly responsible for decreased resting cardiac output. Reduction in plasma renin activity and urinary aldosterone excretion is also observed after clonidine, likely related to reduction in renal SNA 9–11 …”

“…Treatment with oral clonidine has been shown to decrease resting cardiac output by 15% to 20% without affecting total peripheral resistance (TPR) in hypertensive patients 8,9 . Reduction in heart rate, rather than stroke volume, is mainly responsible for decreased resting cardiac output.…”