PubMed Health⌕ Search

Biomedical subjects

J Conway

Publications and source records attributed to J Conway.

11 recordsLinked to original sources
PubMed1978

Aging and the cardiovascular system.

With advancing age blood pressure rises in most populations with the exception of some isolated tribes. In western countries 30 to 40% of the people above the age of 60 years have casual blood pressure levels greater than or equal to 160/95 mm Hg. Advancing age per se produces a number of physiological changes related to blood pressure, such as a decrease in cardiac output, an increase in peripheral vascular resistance and a decrease in plasma renin-angiotensin-aldosterone levels. The mechanism causing the elevation in pressure with age are unknown though increased rigidity of the great vessels contributes to the rise in systolic pressure. There is a decline in the sensitivity of the baroreceptor reflex, but the contribution of this to the elevation of pressure has not be elucidated. Elderly patients with uncomplicated essential hypertension have a low cardiac output and high peripheral vascular resistance. The rise in blood pressure is associated with an increased cardiovascular morbidity and mortality even in the elderly hypertensives. The available data on the efficacy of hypotensive treatment in the elderly is scanty. There are no data proving that hypotensive therapy prolongs life. Controlled studies on the prevention of organ damage especially cerebrovascular accidents are inconclusive, showing either a significant decrease or no effect. Isolated reports illustrate, however, that drastic blood pressure reduction can provoke serious side effects, thus decreasing the quality of life. Hypotensive treatment is indicated in elderly hypertensive patients with hypertensive retinopathy grade III or IV, congestive heart failure or cerebral haemorrhage, in elderly patients with a markedly elevated diastolic blood pressure (greater than or equal to 120 mm Hg) and a trial of hypotensive therapy should be offered in milder forms of hypertension when it is accompanied by certain specific symptoms such as angina, headache and dyspnoe. The management of elderly hypertensive patients is more difficult than in the young. General measures are often not well accepted. The dose adjustment of the hypotensive agent is more critical and volume depletion or orthostatic hypotension are more likely to occur.

Aged↗
PubMedDate not supplied

The influence of the intrinsic sympathomimetic activity of beta-adrenoceptor antagonists on haemodynamic effects in anaesthetized dogs.

1. The effects of propranolol, atenolol (ICI 66,082), practolol and pindolol on heart rate and maximal left ventricular dp/dt, atrioventricular conduction time, mean aortic flow and diastolic blood pressure during cardiac pacing were investigated over a wide dose range (0.025-4.0 mg/kg, i.v.) in dogs anaesthetized with pentobarbitone.2. Propranolol and atenolol produced similar reductions in haemodynamic parameters. Propranolol had no further effect in dogs pretreated with atenolol. 3. Practolol tended to cause smaller reductions in the haemodynamic parameters than either propranolol or atenolol. Subsequent administration of propranolol still had some depressant activity. 4. Pindolol produced a biphasic response, with depression of cardiac function at the low doses (0.025 and 0.1 mg/kg), but a reversal of effect as the dose was increased. 5. It is therefore concluded that, in anaesthetized dogs, the intrinsic activity of practolol and pindolol limits the fall in heart rate, cardiac conduction, aortic flow and maximal dp/dt observed with beta-adrenoceptor blockade. With pindolol, however, the influence of intrinsic activity is observed only in high doses related to beta-adrenoceptor blockade.

Adrenergic beta-Antagonists↗
PubMedDate not supplied

The role of angiotensin in the control of blood pressure during sodium depletion.

Sodium depletion was induced in dogs to raise plasma renin activity (PRA) from 1.11 to 26.48 ng/ml/hr. Little overall change in blood pressure (BP) occurred, but cardiac output (CO) and central venous pressure fell, while total peripheral resistance and heart rate (HR) increased. A nonapeptide converting enzyme inhibitor (CEI) produced a fall in BP which was linearly related to log. PRA; the intercept with PRA was at 1.05 ng/ml/hr, close to the average value for dogs on a normal diet. The fall in BP with this agent was not accompanied by an increase in HR or CO. When Sar1-Ala8 angiotensin II was used to antagonize the action of angiotensin, the fall in BP was also linearly related to log. PRA. However, for a given level of PRA this fall in BP was less than that achieved with CEI and the intercept of BP fall with PRA was 2.6 ng/ml/hr. Again with this agent there was little change in HR or CO as BP was reduced. Thus, both antagonists lowered peripheral resistance without exciting the homeostatic reflexes indicating that, as PRA rose above the normal resting level, the angiotensin generated had both a direct and indirect effect in maintaining BP.

Angiotensin II↗