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Query: UMLS:C0020473 (hyperlipidemia)
 15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The study objective was to determine the effects of monotherapy with clonidine and atenolol versus placebo on serum lipids, apolipoproteins, and blood pressure in patients with mild primary hypertension. The protocol comprised a double blind, randomized, placebo-controlled 5-month prospective study carried out in an outpatient general internal medicine clinic in a university medical center. There were 92 patients ages 18 to 70, with mild primary hypertension (sitting diastolic blood pressure of greater than 90 mm Hg and less than 105 mm Hg) without significant cardiac, renal, cerebrovascular, hepatic, neoplastic, or hematologic disorders. Patients with severe hyperlipidemia or peripheral vascular disease were also excluded. All factors known to effect serum lipids were held constant throughout the study (i.e., diet, weight, exercise, caffeine, tobacco). Atenolol and clonidine significantly reduced blood pressure when compared with placebo. Atenolol caused significant increases in serum triglycerides and apolipoprotein B (p less than 0.05) and significant reductions in high-density lipoprotein-cholesterol, apolipoproteins A-I and A-II (p less than 0.05). Atenolol also induced a significant adverse effect on all lipid ratios, increasing total cholesterol/high density lipoprotein-cholesterol, low density lipoprotein-cholesterol/high density lipoprotein-cholesterol, apolipoprotein B/apolipoprotein A-I and apolipoprotein B/apolipoprotein A-II ratios and decreasing low density lipoprotein-cholesterol/apolipoprotein-B ratio (p less than 0.05). Clonidine caused significant reductions in high-density lipoprotein-cholesterol, apolipoproteins AI and AII (p less than 0.05 but was neutral on all other lipids, lipid subfractions, and apolipoproteins. Clonidine did not significantly alter any of the lipid ratios.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effects of clonidine hydrochloride versus atenolol monotherapy on serum lipids, lipid subfractions, and apolipoproteins in mild hypertension. 219 93

This review presents our new findings regarding the centrally-induced effects of histamine and clonidine. We have found for the first time that histamine administered intracerebroventricularly (icv) induces a dose-related increase in serum free fatty acids (FFA) in conscious rats. Both H1 and H2 receptors participate in this stimulation. Histamine interacts with central alpha 1 and beta-adrenoceptors and with cholinergic muscarinic receptors when inducing hyperlipemic response in non-stressed rats. Clonidine given icv induces also hyperlipemia which, as shown by us, is elicited by a central alpha 2-adrenergic mechanism. In hypothermia caused in rats by clonidine not only already known central alpha-adrenergic but also an H2-histaminergic mechanism participates to an equal extent. We have found for the first time that in conscious rats both under normal and stress conditions not only central histamine H1- but also H2-receptors mediate the stimulation of the pituitary-adrenocortical response measured indirectly through corticosterone secretion. In our study evidence has for the first time been obtained that in non-stressed rats brain histaminergic mechanism interacts with alpha 1, alpha 2- and beta-adrenoceptors and with cholinergic muscarinic receptors when stimulating the pituitary-adrenocortical response. By contrast, in stressed animals central histamine H1- and H2-receptors interact with alpha 1- and alpha 2- but not beta-adrenergic and cholinergic muscarinic receptors when increasing the corticosterone response. We have also demonstrated that in contrast to a known inhibitory action on adrenocortical secretion in anesthetized dogs, clonidine given icv increases the corticosterone response in both non-stressed and stressed rats by stimulating alpha-adrenoceptors. In stressed animals this effect of clonidine is also mediated, to an equal extent, by H2-receptor mechanism. Our data strongly suggest that in some central effects clonidine affects both alpha 2 and H2 receptor mechanism. This challenges the view that clonidine is a selective alpha-adrenergic agonist.
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PMID:Central metabolic and pituitary-adrenocortical stimulatory action of histamine and clonidine. 608 56