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Biomedical subjects

D F Horrobin

Publications and source records attributed to D F Horrobin.

At least 361 records · Page 20Linked to original sources
PubMed1976

Vascular actions of frusemide and bumetanide on the rat superior mesenteric vascular bed: interactions with prostaglandins.

1. The addition of frusemide or bumetanide to perfusion fluid inhibited the response of the isolated mesenteric vascular bed to noradrenaline. 2. Addition of prostaglandin E2 to the perfusion fluid completely restored the response to noradrenaline. 3. Inhibition of prostaglandin secretion by indomethacin with restoration of responses to noradrenaline by the addition of exogenous prostaglandin E2 prevented the inhibitory effect of frusemide or bumetanide on responses to noradrenaline. 4. The inhibitory effects of diuretics on responsiveness to noradrenaline is mediated by blockade of endogenous prostaglandin synthesis.

Animals↗
PubMed1976

The effect of prolactin on the response of human lymphocytes to phytohaemagglutinin.

Lymphocytes were collected from ten normal human males and incubated with or without phytohaemagglutinin (PHA) in the absence or presence of ovine prolactin in concentrations found in normal individuals and in human pregnancy. Prolactin consistently inhibited lymphocyte transformations. The degree of inhibition became progressively less as PHA concentrations were increased.

Depression, Chemical↗
PubMed1976

Vascular actions of furosemide and bumetanide on the rat superior mesenteric vascular bed: interactions with prolactin and prostaglandins.

The mesenteric vascular bed of the rat was used to investigate the effects of furosemide, bumetanide, prolactin, aspirin, indomethacin and prostaglandin E2 on the pressor response to norepinephrine. Furosemide, bumetanied and indomethacin could all inhibit the responses to norepinephrine: in each case responsiveness was restored by the addition of prostaglandin E2 to the perfusate. Bumetanide and furosemide both failed to inhibit responsiveness in the presence of an adequate amount (50 pg/ml) of prostaglandin E2. As has been shown previously, ovine prolactin in a concentration of 50 ng/ml enhanced pressor responses to norepinephrine while 500 ng/ml, after an initial potentiation, inhibited responsiveness. Aspirin, furosemide and bumetanide all reversed both the potentiation produced by the lower prolactin concentration and the inhibition produced by the higher one. When taken in conjunction with other evidence these results suggest that the diuretics exert their vascular effects by inhibiting prostaglandin synthesis whereas prolactin acts by stimulating such synthesis.

Animals↗
PubMed1976

Physiological cortisol levels block the inhibition of vascular reactivity produced by prolactin.

Cortisol in concentrations similar to the unbound levels of the hormone in human plasma can reverse the inhibition of vascular reactivity produced by prolactin. In the rat mesenteric vascular bed, cortisol alone in similar concentrations had no significant effect on the pressor responses to norepinephrine: the action of cortisol was seen only when prolactin was present. The relationships between the effects of different concentrations of prolactin and cortisol suggest that at some point there is a competitive interplay between the effects of the two hormones. There is indirect evidence that this interplay is at the level of prostaglandin synthesis or release. We suggest that cortisol has no effect on basal prostaglandin production but blocks the synthesis or release occurring in response to polypeptide hormone stimulation.

Animals↗
PubMed1975

Seasonal and sexual variations in the responsiveness of rabbit hearts to prolactin.

Rabbit hearts perfused by the Langendorff technique were studied. The addition of ovine prolactin (NIH-P-S-10) to the perfusate in a concentration of 50 ng/ml produced rapid increases in both the amplitude and rate of contraction in 33 adult male hearts studied in winter. Prepubertal male animals showed no response, and only 1 out of 12 adult females responded. Pretreatment for 10 days with 2.5 mg/day testosterone propionate led to minimal inotropic but not chronotropic responses in 2 out of 4 prepubertal males and 2 out of 4 adult females to prolactin. Clear responses to prolactin were seen in 5 adult males pretreated with reserpine. Propanolol consistently reversed both the inotropic and chronotropic actions of prolactin. The original experiments were performed in January and February. When tested in May, adult males failed to respond to prolactin and this situation, persisted until October when responsiveness again appeared. The same prolactin preparation and procedures were used throughout indicating that the changes must have been due to seasonal variations in the cardiac responsiveness to the hormone.

Animals↗