Non-neural electrical responses of smooth muscle cells of the rabbit basilar artery to electrical field stimulation.

Abstract

In smooth muscle cells of the rabbit basilar artery, field stimulation evoked a depolarizing response which consisted of a fast (1-3 s duration) and a following slow (1-4min duration) component. The amplitude of these responses increased in an intensity-dependent manner and, when exceeding 10-15 mV, a spike potential was generated. During generation of the slow depolarization, ionic conductances of the membrane were increased. When outward current pulses with long duration (2-3 s) were applied to the smooth muscle using the partition stimulating method, electrotonic potentials and spike potentials were generated. The cessation of the current pulse caused repolarization of the membrane with time constant of 250-350 ms. The depolarizing responses were resistant to tetrodotoxin, sympathetic transmission blocking agents (guanethidine, bretylium, or 6-hydroxydopamine treatment), receptor antagonists for 5-hydroxytryptamine (methysergide), dopamine (haloperidol), ACh (atropine), noradrenaline (phentolamine), ATP (a,f-mATP) or histamine (mepyramine), blockade of synthesis of prostaglandins or thromboxane A2 (indomethacin) or high Mgt + j low Cat + solution. Smooth muscle cell membrane of the basilar artery was depolarized by 5-hydroxytryptamine (above 0.1 µM) or histamine (above 10 µM) but not by ACh (up to 100 µM) or noradrenaline (up to 10 µM). The depolarization induced by 5-hydroxytryptamine or histamine was antagonized by methysergide or mepyramine, respectively. Denervation of the vessel by storing in a cold condition (4°C) decreased but did not abolish the depolarizing response. The decrease in amplitude of the depolarizing response during cold storage was attributed to associated depolarization of the smooth muscle membrane. Internal perfusion of the vessel with distilled water abolished generation of the depolarizing response, and this procedure also abolished the endothelium-dependent relaxation induced by ACh during the potassium contraction. The results suggest that the depolarizing response evoked by field stimulation is generated by substances released from nonneural components, possibly from the endothelial cells.

Factors inducing endothelium‐dependent relaxation in the guinea‐pig basilar artery as estimated from the actions of haemoglobin

“…In the basilar artery, multiple substances may be released during activation of endothelial cells, not only EDRF and EDHF but also endotheliumderived contracting factor (De Mey & Vanhoutte, 1983;Nagao & Suzuki, 1987) and also relaxing substances, such as prostacyclin (PGI2) (Moncada et al, 1977;Baenziger et al, 1977;Eldor et al, 1981;Domae & Kuriyama, 1986). It is unlikely that the effects of ACh on the guinea-pig basilar artery can be accounted for by the release of PGI2 since the relaxant response to ACh is unchanged by indomethacin and PGI2 does not hyperpolarize the membrane (unpublished observations).…”

Calcium dependency of the endothelium‐dependent hyperpolarization in smooth muscle cells of the rabbit carotid artery.

“…As there are gap junctions between endothelial and adjacent smooth muscle cells (Rhodin, 1967;Taugner, Kirchheim & Forssmann, 1984), electrical coupling between these two types of cells may occur . In fact, the non-neuronal depolarizing responses elicited by electrical field stimulation in smooth muscle cells of the rabbit basilar artery are not generated after removal of the endothelium (Nagao & Suzuki, 1987). However, evidence that the hyperpolarization of smooth muscle cells in tissues with no endothelium can be produced indirectly (i.e.…”

Airway epithelial cells regulate membrane potential, neurotransmission and muscle tone of the dog airway smooth muscle.

“…However, in the mechanically agitated bronchioles, almost all the examined sections (95%) had lost 60-90% of the epithelial luminal surface. We also used hypo-osmolarity shock to destroy the epithelial layer, as is done for endothelial cells in blood vessels (Bolton, Lang & Takewaki, 1984;Nagao & Suzuki, 1987). Histological examination of the bronchioles revealed that the epithelial luminal surface was completely destroyed after the hypo-osmolarity shock, as has been noted in blood vessels (Nagao & Suzuki, 1987).…”

“…The fixed needle was also used for electrical stimulation of ring preparations of the bronchiole. As required for the study, the epithelial cells were removed mechanically by rubbing the internal surface of the bronchioles with a fine silver wire (200 ,Im diameter) or by hypo-osmolarity shock by exposing the inner lumen of the bronchioles to distilled water for about 30-60 s as has previously been done in vascular tissues for removal of endothelial cells (Bolton et al 1984;Nagao & Suzuki, 1987).…”