Biomedical subjects

H Houben

Publications and source records attributed to H Houben.

26 records · Page 2Linked to original sources

PubMed1983

Hemodynamic and humoral effects of coffee after beta 1-selective and nonselective beta-blockade.

Several studies report a substantial rise in plasma catecholamines after caffeine. Epinephrine infusion induces a pressor response after nonselective beta-blockade. We studied the hemodynamic and humoral effects of drinking coffee after placebo and after both nonselective (propranolol) and beta 1-selective (metoprolol) blockade in 12 normotensive subjects. After placebo, coffee induced a rise in systolic and diastolic blood pressure and a fall in heart rate, whereas forearm blood flow did not change. Plasma catecholamines, especially epinephrine (+150%), rose and plasma renin activity, fell after drinking coffee. The effects of coffee on blood pressure, forearm blood flow, and all humoral parameters were not altered by pretreatment with propranolol or metoprolol. The fall in heart rate after coffee, however, seemed to be greater during propranolol. We conclude that the rise in plasma epinephrine after coffee was too small to reveal differences in reaction in propranolol- and metoprolol-pretreated subjects.

Adolescent↗

PubMed1983

Hemodynamic effects of isometric exercise and mental arithmetic in hypertension treated with selective and nonselective beta-blockade.

Hypertensive patients have an unfavorable pressor response to exogenous epinephrine during nonselective beta-blockade. We studied hemodynamics during epinephrine release induced by handgrip exercise and mental arithmetic to examine the clinical relevance of this phenomenon. Twenty-two hypertensive patients were examined in a double-blind crossover experiment with placebo, propranolol (240 mg daily), placebo-washout, and metoprolol (300 mg daily). Changes induced by stress tests for systolic and diastolic blood pressure, heart rate (HR), and forearm blood flow (FBF) were of the same order on both beta-blockers. Rises in HR and FBF were equally reduced by both drugs. Neither handgrip exercise nor mental arithmetic induced significant differences in reaction during selective and nonselective beta-blockade.

Adolescent↗

PubMed1982

Effect of low-dose epinephrine infusion on hemodynamics after selective and nonselective beta-blockade in hypertension.

We studied hemodynamic effects of low doses of epinephrine in five hypertensive patients receiving long-term treatment with propranolol and metoprolol. Epinephrine was infused at graded rates of 0.5, 1.0, 2.0, and 4.0 micrograms/min. During propranolol treatment epinephrine induced a marked pressor effect at all rates. There was a considerable rise in systolic as well as in diastolic blood pressure and heart rate fell. During metoprolol treatment there was only a slight rise in blood pressure and heart rate rose. Forearm blood flow was decreased by epinephrine during propranolol. Calculated forearm vascular resistance showed opposite effects. We conclude that infusion of small doses of epinephrine results in a marked difference in reaction in propranolol- and metoprolol-treated patients and that this may have relevance in the choice of beta blocker to be used in the treatment of hypertension.

Adrenergic beta-Antagonists↗

PubMed1982

Effects of cold exposure on blood pressure, heart rate and forearm blood flow in normotensives during selective and non-selective beta-adrenoceptor blockade.

Haemodynamic effects of a cold pressor test (foot immersion for 6 min in water at 5 degrees C) without medication and after the non-selective beta-adrenoceptor blocker propranolol and the selective beta-adrenoceptor blocker metoprolol were studied in 17 volunteers. In the control study as well as in the study with the beta-adrenoceptor blockers cold exposure caused comparable changes, namely a blood pressure rise and a reduction of forearm blood flow. The increase in heart rate during cold exposure was clearly and equally reduced by both beta-adrenoceptor blockers. Plasma noradrenaline rose significantly by 47%, plasma adrenaline did not change. It is concluded, that as to this kind of stress, beta 1-selective-adrenoceptor blockade confers no important advantage over non-selective beta-adrenoceptor blockade.

Adolescent↗

PubMed1981

Haemodynamic effects of cigarette smoking during chronic selective and non-selective beta-adrenoceptor blockade in patients with hypertension.

1 Haemodynamic effects of cigarette smoking before and during chronic treatment with propranolol and metoprolol were studied in 16 patients with essential hypertension. 2 Smoking of cigarettes induced an increase in blood pressure of the same degree in all experimental sessions. Heart rate increased by 16 beats/min during smoking alone, but increased significantly less, when a beta-adrenoceptor blocker was used. Forearm blood flow decreased during smoking in both medication periods. 3 Plasma adrenaline rose significantly during smoking from 0.37 nmol/l to 0.77 nmol/l; plasma noradrenaline did not change. 4 It is concluded that the blood pressure changes induced by smoking are not essentially altered during chronic treatment with selective or non-selective beta-adrenoceptor blockade. Only the increase in heart rate is significantly less pronounced during treatment with both drugs.

Adolescent↗

PubMed1979

Influence of selective and non-selective beta-adrenoreceptor blockade on the haemodynamic effect of adrenaline during combined antihypertensive drug therapy.

1. Haemodynamic effects of adrenaline were studied in 27 hypertensive patients, succesively during treatment with propranol and metoprolol. In 12 patients beta-adrenoreceptor blockade was combined with diuretics and in 15 patients the blockade was combined with vasodilators. 2. During propranolol adrenaline caused a marked pressor effect: there was a considerable rise in systolic as well as in diastolic blood pressure and a marked fall in heart rate. During metoprolol there was only a slight rise in blood pressure and an increase in heart rate. 3. Forearm blood flow was decreased by adrenaline during propranolol and was increased during metoprolol. Calculated vascular resistance showed opposite changes. 4. Results were essentially the same when beta-adrenoreceptor blockade was combined with diuretics or with vasodilators and did not differ from previous results obtained in patients treated by blockade alone. 5. If adrenaline infusion can be considered as a model for acute stress, our results seem to favour a selective beta 1-adrenoreceptor blocking agent over a non-selective one, even when the blocker is combined with a diuretic or a vasodilator.

Adult↗

PubMedDate not supplied

Effect of the bombesin receptor blockers [Leu13, psi CH2NH-Leu14]bombesin and N-pivaloyl GRP(20-25) alkylamide (L 686,095-001C002) on basal and neuromedin C-stimulated PRL and GH release in pituitary cell aggregates.

Perifusion of rat anterior pituitary cell aggregates, cultured in estrogen-supplemented serum-free medium with 1 nM of the bombesin (BBN)-like peptide, neuromedin C (NMC), significantly stimulates GH and PRL release. This effect is dose-dependently inhibited by the BBN receptor blocker L 686,095-001C002 [an N-pivaloyl-gastrin-releasing-peptide(20-25) alkylamide]. The IC50 was 0.20 nM in the case of the GH response and 0.16 nM in the case of the PRL response. The antagonist has no effect on basal PRL or GH release. [Leu13, psi CH2NH-Leu14]BBN (psi BBN) displays an IC50 of 0.41 microM for inhibiting the GH response and 0.36 microM for inhibiting the PRL response to NMC. At a concentration of 0.5 microM or 5 microM, however, the latter antagonist stimulates PRL and GH release when perifused alone. This stimulatory effect is dose dependent, augments when aggregates are cultured in 1 nM E2 (as is the case for NMC) and is abolished by 2 nM L 686,095-001C002. It is concluded that L 686,095-001C002 is a potent and pure antagonist of pituitary BBN receptors mediating PRL and GH release, whereas psi BBN is a relatively weak antagonist with considerable partial agonist activity.

Amides↗

PubMedDate not supplied

Unexpected effects of peptide and nonpeptide substance P receptor antagonists on basal prolactin and growth hormone release in vitro.

The effect of peptide and nonpeptide substance P antagonists on prolactin (PRL) and growth hormone (GH) secretion was evaluated in three-dimensional rat anterior pituitary cell aggregates. [D-Arg1,D-Phe5,D-Trp7,9,Leu11]Substance P inhibited basal growth hormone (GH) release at a concentration range of 1-10 microM. At higher concentrations (50 microM), the analogue inhibited basal prolactin (PRL) release but provoked a tenfold stimulation of GH release. However, these latter two effects could neither be mimicked nor antagonized by the tachykinins substance P (10 microM), neurokinin A (10 microM), and neurokinin B (3.3 microM). The effects could also not be explained by agonism or antagonism at the level of other receptors (e.g., vasopressin, bombesin, angiotensin II, thyroid hormone-releasing hormone, vasoactive intestinal peptide, dopamine, adrenaline, acetylcholine). Remarkably the nonpeptide substance P antagonists R 30732 (10 microM), R 32602 (10 microM), and CP-96,345 (10 microM) showed a similar inhibition of PRL release and a stimulation of GH release. At a one hundredfold lower concentration, sufficient to block substance P receptors in other tissues. CP-96,345 did not affect PRL or GH release. It is concluded that substance P antagonists, when used at high concentrations, have profound intrinsic activities on PRL and GH release that are not mediated by substance P receptors. The failure of the more potent substance P antagonist, CP-96,345, to influence basal PRL or GH release when used at lower concentrations suggests that endogenous substance P in the anterior pituitary does not play a tonic paracrine role on GH or PRL secretion.

Amino Acid Sequence↗