dihydroergotoxine and Hypertension--Renal

The experimental evidence reviewed in this article suggests that the kidneys may have an additional function in regulating blood pressure besides their role in controlling both blood volume by urine formation and the relative state of vasoconstriction by the renin-angiotensin system. That is, the kidneys may have an additional influence upon the vasculature of a hormonal vasodilating system. The interstitial cells of the renal medulla appear to be mediating this activity and lipid compounds have been extracted from the renal medulla which display depressor activity. One such compound, the antihypertensive polar renomedullary lipid (APRL), has been demonstrated to consist of specific alkyl ether analogues of phosphatidylcholine. The vascular responses to these compounds include vasodilation of both arterioles and venules, rapid lowering of arterial blood pressure with little or no tachycardia, increased depressor activity in hypertensive animals, and blockade of vascular smooth muscle alpha 1-adrenergic receptors. Most recently, APRL and a synthetic analogue, 1-0-octadecyl-2-acetyl-sn-glycero-3-phosphorylcholine, have been used to demonstrate alpha-adrenergic receptor blockade on a smooth muscle cell line (DDT1) by radioligand assays. This action may be due to the insertion of these compounds into cell membranes causing subsequent steric interactions and blockade of the alpha-adrenergic receptor.

Topics: Acetylation; Adrenergic alpha-Antagonists; Animals; Arterioles; Binding, Competitive; Blood Pressure; Blood Volume; Cell Line; Dihydroergotoxine; Glycerylphosphorylcholine; Humans; Hypertension, Renal; Kidney; Kidney Medulla; Muscle, Smooth; Norepinephrine; Phosphatidylcholines; Receptors, Adrenergic; Receptors, Adrenergic, alpha; Vasodilation; Veins

Topics: Animals; Binding Sites; Blood Pressure; Cardiomegaly; Cardiovascular System; Dihydroergotoxine; Hypertension; Hypertension, Renal; Kidney; Lung; Membranes; Rats; Receptors, Adrenergic; Receptors, Adrenergic, alpha; Receptors, Adrenergic, beta

Dihydroergotoxine (DHET) perfused in the dog (100 microgram/kg) presenting a cerebral per-hypocapno-anemic syndrome reduces cerebral hyperemia, increases cerebral venous PO2, despite the rise in CMRO2 and favors glucose oxidation by the brain. DHET (20 mg/kg p.o.) is able to drop mean, diastolic and systolic arterial blood pressures in renal-hypertensive rats having a cerebral edema induced by triethyltin intoxication without affecting cerebral water and sodium levels which are increased in the controls. DHET (50 microgram/kg i.v.) can also improve EEG changes produced by a traumatic edema but does not exert (200 microgram/kg i.v.) any effect on EEG changes produced in the rabbit by lithium chloride intoxication.

Topics: Anemia; Animals; Blood Gas Analysis; Blood Glucose; Brain; Brain Edema; Cerebrovascular Circulation; Dihydroergotoxine; Disease Models, Animal; Dogs; Electroencephalography; Electrolytes; Hypertension, Renal; Hyperventilation; Hypoxia, Brain; Lactates; Lithium; Oxygen Consumption; Rabbits; Triethyltin Compounds