Biomedical subjects
R B Strecker
Publications and source records attributed to R B Strecker.
Tiotidine, a new H2-receptor antagonist, is a potent inhibitor of nocturnal acid secretion in duodenal ulcer patients.
The efficacy of tiotidine, a new H2-receptor antagonist, in reducing nocturnal acid secretion of duodenal ulcer patients (N = 12, ages 21-60 years) was investigated. Different doses of tiotidine, 25, 50, 100, and 150 mg or placebo, were given as a single oral dose and acid secretion collected overnight. Tiotidine produced a significant, prolonged, and dose-related reduction of the nocturnal acid secretion without important side effects. The inhibition of cumulative H+ secretion after 25, 50, 100, and 150 mg tiotidine was 80, 89, 96, and 98% of that observed after placebo, while 300 mg of cimetidine caused an 87% inhibition. Compared to cimetidine, tiotidine appears to be approximately eight times more potent on a molar basis than cimetidine as an inhibitor of acid secretion, and the tiotidine effect is more prolonged. This strong and safe H2-receptor antagonist may be an important addition to the treatment of acid hypersecretory states.
Dissociation constant of the norepinephrine-receptor complex in normotensive and hypertensive rats.
Previous reports have suggested that smooth muscle obtained from the thoracic aorta of spontaneously hypertensive rats is less responsive to vasoconstrictive agents than that obtained from normotensive rats. The present study was undertaken to determine whether the responsiveness of aortic muscles from normotensive and spontaneously hypertensive rats correlates with a difference in the affinity of the adrenergic receptors for norepinephrine and whether antihypertensive therapy alters the affinity of the adrenergic receptors for norepinephrine. The affinity of the adrenergic receptors for norepinephrine was determined by computing the dissociation constant of the norepinephrine-receptor complex (KDR). The values computed for KDR in aortic muscles from normotensive and spontaneously hypertensive rats that had received no antihypertensive therapy were 1.07 X 10(-7)M and 1.17 X 10(-7)M, respectively. The values computed for KDR in aortic muscles from normotensive and spontaneously hypertensive rats that had received antihypertensive therapy were 1.38 X 10(-7)M and 1.29 X 10(-7)M, respectively. The differences in these values for KDR are not significant. These results indicate that the difference in the contractility of aortic muscles from normotensive and spontaneously hypertensive rats is not related to an alteration in the affinity of the adrenergic receptors for norepinephrine and that the affinity of the adrenergic receptors for norepinephrine is not altered by antihypertensive therapy. Thus, it appears that the etiology of hypertension cannot be directly correlated with a difference in the affinity of the adrenergic receptors for norepinephrine.