Prostaglandins E1, E2 and I2: evidence for three distinct actions in vascular smooth muscle.

In the perfused mesenteric artery of the rat prostaglandins (PGs) E₁, E₂ and I₂ had distinct actions. PGE₂ potentiated pressor responses to noradrenaline, angiotensin II and potassium ions. PGE₁ potentiated responses to noradrenaline and angiotensin at low concentrations and inhibited them at high concentrations: no concentrations had any effect on potassium responses. PGI₂ inhibited responses to noradrenaline and angiotensin but had no effect on potassium responses. These three distinct actions suggest that the binding sites for the three PGs in this vascular muscle must be distinct.     

Changes in coronary vascular resistance associated with prolonged hypoxia in isolated rat hearts: a possible role of prostaglandins

Hypoxia caused an initial dilatation in the coronary circulation of perfused male rat hearts but within 15 minutes the coronary vessels became strongly constricted. In hearts from very young (30 days) animals only dilatation was seen. Physiological levels of progesterone in the perfusate prevented the constriction whereas estradiol and testosterone had little effect. Blockade of adrenergic alpha receptors or angiotensin receptors did not prevent the constriction. Two structurally different inhibitors of prostaglandin synthesis, indomethacin and aspirin, and three drugs which can interfere with prostaglandin action, chloroquine, procaine, and propranolol blocked the constriction. Thromboxane A2, a product of PG synthesis, had been reported to be a coronary vasoconstrictor but four drugs which inhibit thromboxane A2 synthesis, dipyridamole, benzydamine, N-0164 and imidazole were not able to prevent the hypoxia-induced constriction. This form of hypoxic coronary constriction seems not to be related to α-adrenergic, angiotensin or thromboxane A2 effects. It may depend on some other product of the prostaglandin pathway.     

Low prostaglandin concentrations cause cardiac rhythm disturbances. Effect reversed by low levels of copper or chloroquine

IN perfused male rat hearts concentrations of prostaglandins (PGs) E2 and F2α in the range 1 pg/ml to 10 ng/ml (2.8 × 10⁻¹² to 2.8 × 10⁻⁸M) consistently caused rhythm irregularities. Higher concentrations had no effect themselves and stabilized rhythm in hearts made unstable by lower concentrations. Copper ions (as the sulphate) at 2 × 10⁻⁶M stabilized hearts made unstable by PGs and when present prior to the PGs prevented PG induced disturbances. Chloroquine also reversed PG-induced rhythm changes.     

Male pioneering as a mating strategy: the case of the beetle Maladera matrida

1. The phenomenon of male pioneering, whereby males are active (daily) before females, is compared with protandry, a phenomenon whereby males are sexually matured before females. The effects of natural selection and sexual selection on both phenomena are discussed. 2. In Maladera matrida Argaman (Coleoptera: Scarabaeidae), males emerged from the soil a few minutes before females, every evening, to feed and mate. 3. Aggregations of males and females are formed at sites of plant damage where males initiated feeding. 4. All copulations were initiated at the beginning of the activity period so males that emerge earlier may increase their probability of finding a mate. 5. Females mate only once in an evening. 6. Males that emerge later may not find receptive females with which to mate. 7. The aggregation of beetles per se did not contribute to the individual mating success because it occurred during and after the copulating had begun. 8. Male pioneering may evolve through sexual selection by means of male–male competition in time to achieve receptive females.