An increase in putative voltage dependent calcium channel number following reserpine treatment

Powers, Robert D.; Colucci, Wilson S.

doi:10.1016/0006-291x(85)91208-2

Cited by 14 publications

(2 citation statements)

References 9 publications

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“…Consistent with this, our results indicate that reserpine treatment increases the sensitivity of the aorta to an exogenous activator of the calcium channel. It has also been shown that reserpine treatment increases the number of calcium channels in rat seminal vesicles [26], An increase in the number of calcium chan nels of the rabbit aorta could also account for the increase in responsiveness to BAY K 8644 seen after reserpine.…”

Section: Discussionmentioning

confidence: 96%

Effects of Calcium Channel Activators on the Response of Rabbit Aortic Rings to Alpha<sub>1</sub>-Receptor Agonists: Evidence for Two Modes of Action

1989

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The interaction between activators of the calcium channel and the α₁-adrenoceptor has been studied in isolated rabbit aortic rings. The data obtained in these investigations are not consistent with the idea of a homogenous population of α₁-receptors which trigger contraction via a single pathway. Our results suggest that calcium channel activators reveal two modes of spasmogenic action for α₁-adrenoceptor agonists. Furthermore, we have shown that there may be multiple drug recognition sites on the α₁-receptor.

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Section: Discussionmentioning

confidence: 96%

Effects of Calcium Channel Activators on the Response of Rabbit Aortic Rings to Alpha<sub>1</sub>-Receptor Agonists: Evidence for Two Modes of Action

1989

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“…The contractions of the vas deferens and seminal vesicle in response to norepinephrine were potently inhibited by the dihydropyridine‐calcium channel blockers, nifedipine and (S)‐(+)‐niguldipine, indicating the participation of calcium influx through L‐type calcium channels in the contractions resulting from α 1 ‐AR activation. In fact, electrophysiological and radioligand binding assays have shown the presence of L‐type calcium channels in the smooth muscle cells from rat and human vas deferens and seminal vesicle [16,23–28].…”

Section: Discussionmentioning

confidence: 99%

Investigation of the Effects of α1-Adrenoceptor Antagonism and L-Type Calcium Channel Blockade on Ejaculation and Vas Deferens and Seminal Vesicle Contractility in Vitro

Kiguti

Pupo

2012

The Journal of Sexual Medicine

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Introduction Premature ejaculation is one of the most common male sexual dysfunctions. Current pharmacological treatments involve reduction in penile sensitivity by local anesthetics or increase of ejaculatory threshold by selective serotonin reuptake inhibitors. α1-Adrenoceptors (α1-ARs) and L-type calcium channels are expressed in the smooth muscles of the male reproductive tract, and their activations play an important role in the physiological events involved in the seminal emission phase of ejaculation. Aim To evaluate if the inhibition of the contractility of the vas deferens and seminal vesicle by α1-AR antagonism or the L-type calcium channel blockade can delay ejaculation. Methods The effects of the α1-AR antagonist tamsulosin and of the L-type calcium channel blockers, nifedipine and (S)-(+)-niguldipine, on contractions induced by norepinephrine in the rat vas deferens and seminal vesicles in vitro and on the ejaculation latency of male rats in behavioral mating tests were evaluated. Main Outcome Measure Tension development of vas deferens and seminal vesicles in response to norepinephrine in vitro and behavioral mating parameters were quantified. Results Tension development of vas deferens and seminal vesicle to α1-AR activation was significantly inhibited by tamsulosin, nifedipine, and (S)-(+)-niguldipine. Tamsulosin displayed insurmountable antagonism of contractions induced by norepinephrine in the rat vas deferens and seminal vesicle. Ejaculation latency of male rats was not modified by tamsulosin, nifedipine, or (S)-(+)-niguldipine; however, both the number and weight of the seminal plugs recovered from female rats mated with male rats treated with tamsulosin were significantly reduced. Conclusion Seminal emission impairment by inhibition of vas deferens or seminal vesicle contractility by L-type calcium channel blockade or α1-AR antagonism is not able to delay the ejaculation.

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Calcium channels and calcium channel antagonists

Greenberg

1987

Annals of Neurology

135

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Changes in free intracellular Ca2+ levels provide signals that allow nerve and muscle cells to respond to a host of external stimuli. A major mechanism for elevating the level of intracellular Ca2+ is the influx of extracellular Ca2+ through voltage-dependent channels in the cell membrane. Recent research has yielded new insights into the physiological properties, molecular structure, biochemical regulation, and functional heterogeneity of voltage-dependent Ca2+ channels. In addition, Ca2+ channel antagonist drugs have been developed that are valuable both as probes of channel structure and function and as therapeutic agents. Preliminary evidence suggests that these drugs may be useful in the treatment of diverse neurological disorders, including headache, subarachnoid hemorrhage, stroke, and epilepsy.

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An increase in putative voltage dependent calcium channel number following reserpine treatment

Cited by 14 publications

References 9 publications

Effects of Calcium Channel Activators on the Response of Rabbit Aortic Rings to Alpha<sub>1</sub>-Receptor Agonists: Evidence for Two Modes of Action

Effects of Calcium Channel Activators on the Response of Rabbit Aortic Rings to Alpha<sub>1</sub>-Receptor Agonists: Evidence for Two Modes of Action

Investigation of the Effects of α1-Adrenoceptor Antagonism and L-Type Calcium Channel Blockade on Ejaculation and Vas Deferens and Seminal Vesicle Contractility in Vitro

Calcium channels and calcium channel antagonists

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