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Biomedical subjects

D F Horrobin

Publications and source records attributed to D F Horrobin.

At least 343 records · Page 19Linked to original sources
PubMed1977

Dopamine enhances the action of prolactin on rat blood vessels. Implications for dopamine effects on plasma prolactin.

It has been claimed that dopamine enhances peripheral uptake of prolactin. Dopamine at 2.1 x 10(-9)M, a concentration which had no effect by itself, enhanced both the potentiation of rat mesenteric vascular reactivity caused by 50ng/ml ovine prolactin and the inhibition of reactivity caused by 500ng/ml prolactin. These observations are consistent with the proposal that dopamine can interact peripherally with prolactin.

Animals↗
PubMed1977

Prostaglandin A2 at low rates of infusion restores the antidiuretic effect of vasopressin in lithium-treated rats.

To test the effect of prostaglandin A2 (PGA2) on renal function, infusions of PGA2 (0-7 ng/kg/min), arginine-vasopressin (AVP) (1-25 ng/kg/min) and PGA2 plus AVP were administered to male rats made resistant to the antidiuretic effect of AVP by pre-treatment with lithium. In non-lithium-treated control rats, AVP had its expected antidiuretic action but in lithium-treated rats neither urinary volume nor osmolarity was changed. Prostaglandin A2 alone had no effect on urine output in lithium-treated rats; AVP plus PGA2 infused together evoked a near normal antidiuretic response. This antidiuretic action of PGA2 contrasts with the diuretic action reported by others. However, our infusion rates were 300-4000 times lower than those of other workers and it is suggested that PGs may have opposite actions on the kidney depending on their concentration. The effect of indomethacin (a blocker of prostaglandin synthesis) on urine flow was tested in five groups of rats on different régimes of liquid intake. Urine flow was reduced in the three groups with the highest urine volumes before treatment, and increased in the two groups with the lowest urinary volumes, again indicating that PGs may have both diuretic and antidiuretic actions.

Animals↗
PubMed1977

The possible role of prolactin in pre-eclampsia.

The primary feature of pre-eclampsia is the pregnancy-associated rise in arterial pressure. Oedema and proteinuria also frequently occur. There is increased responsiveness to pressor agents. Prolactin is present in elevated amounts in human pregnancy and is found in very large quantities in amniotic fluid. Prolactin can cause renal retention of fluid and electrolytes, can elevate arterial pressure and can protentiate responses to pressor agents. It is suggested that either elevated prolactin levels or an increased responsiveness to normal prolactin levels may play a key role in the pathogenesis of preeclampsia.

Adult↗
PubMed1976

Chloroquine, quinine, procaine, quinidine, tricyclic antidepressants, and methylxanthines as prostaglandin agonists and antagonists.

Chloroquine, quanine, procaine, quinidine, clomipramine, theophylline, and caffeine have been shown to be strong prostaglandin antagonists and weak agonists. The antagonist effect is clearly demonstrable at concentrations reached in human plasma when the drugs are used therapeutically. This suggests that prostaglandins are important in several situations in which their role has hitherto been unsuspected. New approaches to the development of prostaglandin antagonists and new uses for established drugs are indicated. In a preliminary study chloroquine has been successfully used to close patent ductus arteriosus in three infants.

Antidepressive Agents, Tricyclic↗
PubMed1976

Indomethacin inhibits responses to all vasoconstrictors in the rat mesenteric vascular bed: restoration of responses by prostaglandin E2.

Indomethacin added to the perfusing buffer inhibited pressor responses to noradrenaline, angiotensin II, arginine vasopressin, histamine, serotonin, calcium ions and potassium ions in the male rat mesenteric vascular bed. For every pressor agent the indomethacin concentration which inhibited response amplitude by 50% was about 7 microg/ml (2.1 X 10(-5) M). With every pressor agent, prostaglandin (PG) E2 could restore normal responsiveness in indomethacin-blocked preparations even while the indomethacin was still present in the buffer. The concentration of PGE2 required was proportional to the concentration of indomethacin. Preparations completely inhibited by indomethacin needed about 5ng/ml PGE2 for complete restoration of normal responses. Aspirin and mefenamic acid could also inhibit responses to all pressor agents tested but with these drugs only a partial restoration could be achieved by PGE2.

Angiotensin II↗
PubMed1976

Chloroquine, quinine, procaine, quinidine and clomipramine are prostaglandin agonists and antagonists.

Chloroquine, quinine, procaine, quinidine and clomipramine behave as prostaglandin (PG) antagonists in a rat mesenteric vascular bed preparation. The ID50 concentrations were within the range of therapeutically effective human plasma levels in each case. Antagonism to PGE2 was studied in detail and seemed to be at least in part competitive. The drugs also antagonized the effects of PGs A1, A2, F2alpha and E1. Each drug also had weak prostaglandin agonist activity but only over a very narrow range of concentrations. It is possible that some of the clinical actions of these drugs may depend on blockade or imitation of natural PG effects. The findings suggest new approaches to the search for PG antagonists, a new screening technique for anti-inflammatory drugs and possible new uses for these established drugs. A preliminary study suggests that chloroquine may be successful in closing a patent ductus arteriosus in infants.

Animals↗