Rise In Mean Blood Pressure Research Articles

Changes in plasma norepinephrine after intravertebral artery infusion of saralasin in sodium depleted dogs.

This study was designed to investigate the central action of circulating angiotensin II on the regulation of blood pressure in sodium depleted states. The effects of intravertebral arterial infusion of angiotensin II and [Sar-1, Ala-8] angiotensin II (saralasin) on plasma norepinephrine (NE) were studied in alpha-chloralose anesthetized dogs. Intravertebral arterial infusion of angiotensin II (10 ng/kg/min) increased mean arterial pressure (MAP), heart rate (HR) and plasma NE. Plasma NE was decreased by intravertebral arterial infusion of saralasin (0.40 +/- 0.05 to 0.28 +/- 0.04 ng/ml, p less than 0.05) in normal dogs. The administration of furosemide produced significant increases in plasma NE (142.4 +/- 23.7%, p less than 0.01), plasma renin activity (PRA) (158.6 +/- 26.3%, p less than 0.01) and HR (32.3 +/- 6.0 beats/min, p less than 0.01). A slight rise in mean blood pressure (3.9 +/- 1.2 mmHg, p less than 0.05) was observed during the furosemide administration. Saralasin infused into the vertebral artery significantly suppressed the furosemide-induced increases in plasma NE, HR and PRA, and lowered mean arterial blood pressure. Intravenous infusion of the same dose of saralasin produced no changes in arterial blood pressure, HR and plasma NE. These results suggest that the central sympathetic potentiation induced by circulating angiotensin II may contribute to the regulation of blood pressure in sodium and volume depleted states produced by furosemide.

Blood pressure studies in rural and urban Western Samoa.

Blood pressure was measured in the rural and urban male and female Polynesian populations of Western Samoa to determine if differences existed in mean blood pressures or in the prevalence of hypertension between these groups. It was found that, in the urban population, both males and females had higher mean blood pressures and approximately double the prevalence of hypertension found in their rural counterparts. There was an age-related rise in mean blood pressure and in the prevalence of hypertension in all groups. Approximately half of the difference in mean blood pressure and hypertension prevalence between rural and urban groups appeared to be due to difference in adiposity. Age and body mass index were significantly and independently correlated with systolic and diastolic blood pressure in each group. The prevalence of hypertension was greater in obese subjects.

Oral Contraceptives and Blood Pressure

Both cross-sectional and longitudinal analysis of data from 13,358 women showed that oral contraceptive use is associated with a slight but statistically significant (P lesser than .05) rise in mean blood pressure, which is reversible. The age-adjusted proportion of oral contraceptive users with a blood pressure over 140/90 mm Hg was about three times that on nonusers. These findings are caused by a uniform upward shift in the blood pressure distribution of oral contraceptive users compared to nonusers. Women continuing oral contraceptive use had no appreciably greater change in blood pressure between two visits than persistent nonusers. The clinical implications of a mild contraceptive-induced blood pressure elevation (systolic, 5 to 6 mm Hg; diastolic, 1 to 2 mm Hg) remain unsettled but disturbing.

Cardiovascular actions of 2,5-dimethoxy-4-methylamphetamine (DOM) in the cat.

The cardiovascular effects of the psychotomimetic DOM were investigated in pentobarbital-anesthetized cats. DOM (1,2 and 4 mg/kg, i.v.) produced a rise in mean blood pressure accompanied by bradycardia. DOM (1 and 2 mg/kg, i.v.) also produced a contraction of the decentralized nictitating membrane. The duration of the pressor response to DOM was reduced in magnitude and duration by hexamethonium, by spinal section plus vagotomy, and by carotid sinus denervation plus vagotomy. Ventricular--cisternal perfusion of 20 mug DOM resulted in a slow developing hypertensive response. Methylsergid significantly attenuated the pressor response and the contraction of the nictitating membrane induced by i.v. DOM administration. The pressor response to DOM was not altered by phentolamine, propranolol or atropine and vagotomy. Bradycardia induced by DOM was antagonized by carotid sinus denervation plus vagotomy, hexamethonium, spinal sectioning plus vagotomy, and propranolol. Bradycardia induced by DOM is therefore a result of a reflex response to increased blood pressure. The present data thus indicate that the pressor response to DOM consists of two compents: a direct vascular effect mediated via the stimulation of serotonergic receptors; and a second pressor effect, mediated by the central nervous system.

The response of the unanesthetized sheep fetus to sympathomimetic amines and adrenergic blocking agents

The response of the unanesthetized intrauterine sheep fetus to sympathomimetic amines was investigated before and after administration of adrenergic blocking agents. Epinephrine, norepinephrine, and methoxamine elicited a prompt increase in systolic and diastolic blood pressures and a decrease in heart rate which tended to be proportional to the rise in mean blood pressure. Isoproterenol, in contrast, produced a fall in arterial blood pressure and a rise in fetal heart rate. The relative changes in blood pressure and in heart rate following the administration of sympathomimetic amines were unaffected by increasing maturity although there was a continuous increase in fetal blood pressure throughout the last trimester of gestation. Phenoxybenzamine (an alpha-receptor-blocking agent) or propranolol (a beta-receptor-blocking agent) exerted only a minor effect on fetal heart rate and blood pressure and did not alter the oxygenation and acid-base state of the fetus. The response to sympathomimetic amines was obliterated. In contrast to the adult of most species, alpha blockade of the fetal sheep did not lead to epinephrine reversal.

Mechanism of pulmonary conversion of angiotensin I to angiotensin II in the dog.

The mechanism of conversion of angiotensin I to angiotensin II was studied in vivo in the pulmonary circulation of the intact anesthetized dog and in vitro in plasma by using L-Leu-anglotensin I, D-Leu-angiotensin I, and des-Leu-angiotensin I which had been synthesized by the solid-phase technique. None of the peptides were active in the rabbit aortic strip preparation; D-Leu-angiotensin I and des-Leu-angiotensin I gave less than 5% of the pressor response of L-Leu-angiotensin I in the pentolinium-treated rat. D-Leu-angiotensin I and des-Leu-angiotensin I were not converted to angiotensin II when incubated with diluted human or dog plasma or partially purified converting enzyme from dog plasma. In a single pulmonary circulation time, following injection of a 20-nmole bolus of L-Leu-angiotensin I into the dog right ventricle, 56% of the material recovered had been converted to angiotensin II, as measured by radioimmunoassay. Conversion was accompanied by a rise in mean blood pressure of 30 mm Hg. After injection of equimolar amounts of D-Leu-angiotensin I and des-Leu-angiotensin I, no generation of angiotensin II and no pressor response occurred. These observations indicate that pulmonary conversion in vivo and plasma conversion in vitro occur via a dipepridylcarboxypeptidase and that a D-amino acid at the C-terminus prevents conversion.

Effects of pH changes on oxygen uptake and plasma catecholamine levels in the dog.

During hypercapnic acidosis induced by ‘apneic oxygenation,’ one observes in the dog a rise in plasma catecholamine levels in the presence of a constant oxygen uptake (Qo2) and a rise in mean blood pressure. When pH is maintained constant or alkaline by infusion of T.H.A.M. (2 amino 2 hydroxymethyl 1–3 propane diol), Qo2 remains constant while plasma catecholamines and blood pressure do not change although total plasma CO2 shows a twofold increase. When blood pH is rapidly shifted from 6.99 ± .03 to 7.52 ± .02, Qo2 increased by 39%, while plasma catecholamine levels were rapidly re-established to normal. The infusion of 1 µg/kg/min. of epinephrine, norepinephrine or isoproterenol will also produce a significant increase in Qo2 and blood pressure in the apneic dog when arterial blood pH is maintained normal or alkaline; but the same dose of epinephrine fails to change significantly Qo2 or blood pressure when arterial blood pH is maintained between 6.97 and 7.28.

Effects of l-epinephrine and l-norepinephrine on foot vasculature after sympathectomy in dogs.

The acutely sympathectomized foot of dogs was less responsive to intra-arterially infused l-epinephrine and l-norepinephrine than the opposite control leg, as indicated by blood flow in the saphenous veins. In chronically sympathectomized legs, blood flow methods failed to disclose any increased sensitivity to intra-arterially or or intravenously infused epinephrine and norepinephrine. The degree of vasoconstriction induced by the two drugs was about equal, as was the rise in mean blood pressure. Blood vessel strips removed from the operated and control legs and tested in vitro responded differently to epinephrine and norepinephrine in that chronically sympathectomized vessels were twice as responsive to the two amines as were the controls. Chronic lumbar sympathectomy undoubtedly produced sensitivity changes in the leg vasculature, and while this was not demonstrable in the intact preparation it could be shown by in vitro studies.