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Biomedical subjects

P Omvik

Publications and source records attributed to P Omvik.

At least 109 records · Page 6Linked to original sources

Long-term effects on central haemodynamics and body fluid volumes of ketanserin in essential hypertension studies at rest and during dynamic exercise.

The long-term haemodynamic effects of ketanserin, a new serotonin-antagonist, was examined in 13 patients of both sexes (age range 24-62 years) with mild and moderate essential hypertension (EH). Cardiac output (CO) and intra-arterial blood pressure (BP) were measured at rest and during exercise before and after nine months of therapy. On ketanserin the mean casual BP was lowered by 15/21 mmHg to 152/91 mmHg and five of the 13 patients became 'normotensive' (BP less than 140/90 mmHg). The intra-arterial systolic pressure fell by 5-8% and the diastolic pressure by 5-11% from pretreatment levels at rest supine, sitting and during 50, 100 and 150 W exercise. The fall in BP was associated with a reduction in CO at rest while during exercise both a fall in CO and in total peripheral resistance contributed to the hypotensive effect. The fall in CO was due to a reduction in heart rate (average: -4 to 8 beats/min). The stroke volume remained unchanged in all settings and oxygen consumption was not affected by the drug. Body weight and body fluid volumes did not change significantly. Eight patients complained of drowsiness and lack of concentration. It is concluded that in mild and moderate EH ketanserin induces a moderate BP reduction associated with a fall in CO. There is no large vasodilating effect after long-term ketanserin treatment either at rest or during exercise. Ketanserin does not influence body fluid balance. The incidence of side-effects is high.

Adult↗

Sodium excretion and blood pressure in middle-aged men in the Sogn County: an intra- and interpopulation study.

Blood pressure (BP) and daily sodium excretion were measured in 262 males aged 35-54 years from three separate districts of the Sogn county in Norway. Averages for mean arterial pressure and sodium excretion were 103.4 mmHg and 192.4 mmol/24 h respectively, which is similar to the excretion rates in most other Western societies. Interpopulation (between groups) analysis revealed statistically significant differences in sodium excretion and BP between the three districts, but no significant correlation was found between individual sodium excretion rates and the respective BPs (within group analysis). The mean urinary sodium/potassium ratio (Na/K) was significantly lower in the district with the lower BP level, but there was no statistically significant correlation between individual Na/K ratios and BP. The lack of significant correlation between sodium excretion and BP in the within group analysis as opposed to the between groups comparison could be due to large intra-individual variation of sodium excretion.

Adult↗

Can left main or proximal left anterior descending coronary artery disease be assessed by non-invasive means?

One hundred consecutive patients with angina pectoris referred for coronary arteriography were studied prospectively for non-invasive assessment of left main (LMCA) or proximal left anterior descending coronary artery (proximal LAD) disease. Evaluation of echocardiographic interventricular septal motion, history and exercise test response could not identify the patients with these specific lesions. It is concluded that LMCA and proximal LAD disease still remain largely unpredictable by non-invasive means.

Adult↗

Pressure natriuresis in hypertension.

Pressure natriuresis, defined as the relationship between sodium excretion and mean arterial pressure (MAP), was assessed during graded reduction of arterial pressure with nitroprusside in 16 essential hypertensives (EH). In all patients, sodium excretion fell linearly with reductions in arterial pressure (r greater than 0.68; p less than 0.05). The per cent change of sodium excretion from control per mmHg change in MAP (delta UNaV/delta MAP) was less in patients with resting MAP above 120 mmHg than in those with lower blood pressure (1.4 +/- 0.1 versus 3.0 +/- 0.3; p less than 0.001), but the pressure at which urine flow extrapolated to zero (75 +/- 3 mmHg) was not significantly different in the two groups. The slope of the relationship between sodium excretion and arterial pressure was significantly correlated with resting MAP (r = -0.67; p less than 0.05) and with plasma volume (r = 0.61; p less than 0.05). Furthermore, the ratio delta UNaV/delta MAP also rose in concert with body fluid volumes when a salt load of 8 g of sodium chloride was added to the regular diet. Thus, the sensitivity of pressure natriuresis was determined by level of resting arterial pressure and body fluid volumes. These experiments suggest tht two mechanisms might be activated in EH to avoid dangerous sodium and volume depletion: 1) attenuation of pressure natriuresis at higher levels of arterial pressure, and 2) blunting of pressure natriuresis by volume contraction. By this hypothesis, the lower slope of pressure natriuresis is secondary to hypertension rather than its cause.

Blood Pressure Determination↗

Effect of sodium depletion on plasma renin concentration before and during adrenergic beta-receptor blockade with propranolol in normotensive man.

Plasma renin levels have been used to discriminate between different forms of hypertension, but how to define the normal range of plasma renin levels has not been agreed upon. Sodium depletion stimulates renin release. Evaluation of plasma renin would, therefore seem possible only in relation to sodium balance. Plasma renin concentration and concurrent daily sodium excretion were determined in 33 healthy normotensive subjects (control group) ingesting high, normal and low sodium diets. A well-defined hyperbolic relationship was found between the two variables indicating that the physiologic level of plasma renin concentration depends on the state of sodium balance. An increase in plasma potassium concentration may reduce plasma renin concentration, but this appeared to be overruled by the stimulating effect of sodium depletion. To examine whether beta-adrenergic stimulation contributes to the increase in plasma renin concentration during sodium depletion, the relationship between plasma renin concentration and concurrent sodium excretion was studied during beta-receptor blockade with propranolol. In 20 healthy normotensive subjects in whom beta-receptor blockade was verified by a significant reduction in pulse rate, the same hyperbolic relationship was found between plasma renin concentration and sodium excretion as in the control group showing that sodium depletion stimulates renin release independent of sympathetic nervous activity.

Adrenergic beta-Antagonists↗

Hemodynamic mechanisms influencing sodium excretion during angiotensin infusion.

To examine mechanisms of transition between antinatriuresis and natriuresis, angiotensin II was first infused intrarenally (0.001-0.07 mug/kg-min) in anesthetized dogs; glomerular filtration rate (GFR), sodium excretion, and intrarenal pressure (IRP), indicating tubular pressure, fell as during mechanical aortic constriction. During supplementary intravenous infusion (0.10-0.30 mug/kg-min), renal blood flow (RBF) rose toward control (tachyphylaxis). Tubular reabsorption increased but was still 17.1% below control. Filtration fraction averaging 0.31 remained constant. Sodium excretion and IRP exceeded control but were normalized by restoring renal arterial pressure mechanically. During intrarenal angiotensin infusion, carotid constriction increased blood pressure more, but RBF, IRP, and sodium excretion less than intravenous angiotensin. Intrarenal infusion of angiotensin at 0.10-0.20 mug/kg-min increased RBF and sodium excretion more in infused than in contralateral kidneys. Thus, angiotensin natriuresis depends on increased perfusion pressure and is augmented as tachyphylaxis develops. High correlation between sodium excretion and IRP at unchanged filtration fraction suggests a regulation of sodium excretion by hydrostatic rather than oncotic pressures in glomerular and peritubular capillaries.

Angiotensin II↗

Renal autoregulation: evidence for the transmural pressure hypothesis.

Autoregulation of glomerular filtration rate (GFR) was examined during uteral orarterial constriction in anesthetized dogs after renal denervation. GFR was sustaineduntil ureteral pressure greater than 80 mmHg, provided renal arterial pressure exceeded 180 mmHg, but fell at ureteral pressure less than 54 mmHg when arterial pressure averaged 127 plus or minus 5 mmHg; renal blood rose as GFR declined. Ethacrynic acid, saline, or mannitol infusion increased tubular pressure without reducing GFR,but during subsequent ureteral constriction GFR fell at uteral pressure less than 40mmHg. During arterial constriction GFR was maintained at lower arterial pressures in hydropenic than in diuretic dogs. Because of thisdifference in the range of autoregulation, saline infusion increased GFR more in hydropenic than in diuretic dogs except at high arterial pressure. This response to reduced plasma oncotic pressure and the constancy of GFR over a wide range of proximal tubular and arterial pressure indicate constancy of thehydrostatic transmural pressure of glomerular capillaries. Afferent arteriolar resistance is, in addition to a regulation by transmural pressure, perhaps controlled by vascular stretch receptors in the glomeruli.

Animals↗

Acute hemodynamic effects of labetalol in severe hypertension.

Intravenous injection of labetalol induced an immediate fall (-22.4%) in blood pressure (BP) in 11 patients with severe hypertension. Hypotensive episodes were avoided by repeated injections of 0.2-0.8 mg/kg. The pressure reduction was associated with a mean fall in total peripheral resistance of 13.6%. Cardiac output fell 10.1% owing to a fall in heart rate of 10.8%, while stroke volume remained virtually unchanged. Despite excellent acute control of BP by intravenous injection, oral labetalol alone or in combination with hydrochlorothiazide was not effective in long-term treatment of these patients with severe hypertension. After 1 week, mean arterial pressure was still 10.4% below the pretreatment level, but after 4 months BP was back to pretreatment level in all except one patient whose BP is still well controlled after more than 2 years on labetalol.

Administration, Oral↗