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Biomedical subjects

Carlos Castillo

Publications and source records attributed to Carlos Castillo.

17 recordsLinked to original sources
PubMed2006

Microvascular blood flow during cardiopulmonary resuscitation is predictive of outcome.

There is growing evidence that microcirculatory blood flow is the ultimate determinant of the outcome in circulatory shock states. We therefore examined changes in the microcirculation accompanying the most severe form of circulatory failure, namely cardiac arrest and the effects of subsequent cardiopulmonary resuscitation. Ventricular fibrillation was electrically induced in nine pigs and untreated for 5min prior to beginning closed chest cardiac compression and attempting electrical defibrillation. Orthogonal polarization spectral imaging was utilized for visualization of the sublingual microcirculation at baseline, 0.5, 1, 3 and 5min after onset of ventricular fibrillation and at 1 and 5min after start of chest compression. Images were also obtained 1 and 5min after restoration of spontaneous circulation. Microvascular flow was graded from 0 (no flow) to 3 (normal flow). Aortic and right atrial pressures were measured and coronary perfusion pressure was computed continuously. Microcirculatory blood flow decreased to less than one-fourth within 0.5min after inducing ventricular fibrillation. Precordial compression partially restored microvascular flow in each animal. In animals that were successfully resuscitated, microvascular flow was significantly greater after 1 and 5min of chest compression than in animals with failed resuscitation attempts. Microvascular blood flow was highly correlated with coronary perfusion pressure (r=0.82, p<0.01). Microvascular blood flow in the sublingual mucosa is therefore closely related to coronary perfusion pressure during cardiopulmonary resuscitation and both are predictive of outcome.

Animals↗
PubMed2006

Effects of estradiol on phenylephrine contractility associated with intracellular calcium release in rat aorta.

The ability of estradiol to affect phenylephrine-induced contraction and the subsequent increase in resting tone, associated with capacitative Ca(2+) entry across the plasma membrane, was evaluated in rat aortic rings incubated in Ca(2+)-free solution. The incubation with estradiol (1-100 nM, 5 min) inhibited both the phenylephrine-induced contraction and the IRT. Neither cycloheximide (1 microM; inhibitor of protein synthesis) nor tamoxifen (1 microM; blocker of estrogenic receptors) modified the effects of estradiol. Estradiol (100 microM) also blocked the contractile response to serotonin (10 microM) but not to caffeine (10 mM). In addition, estradiol (100 microM) inhibited the contractile responses to cyclopiazonic acid (1 microM; selective Ca(2+)-ATPase inhibitor) associated with capacitative Ca(2+) influx through non-L-type Ca(2+) channels. Finally, estradiol inhibited the Ca(2+)-induced increases in intracellular free Ca(2+) (after pretreatment with phenylephrine) in cultured rat aorta smooth muscle cells incubated in Ca(2+)-free solution. In conclusion, estradiol interfered in a concentration-dependent manner with Ca(2+)-dependent contractile effects mediated by the stimuli of alpha(1)-adrenergic and serotonergic receptors and inhibited the capacitative Ca(2+) influx through both L-type and non-L-type Ca(2+) channels. Such effects are in essence nongenomic and not mediated by the intracellular estrogenic receptor.

Animals↗
PubMed2006

Differential expression of alpha1-adrenergic receptor subtypes in coronary microvascular endothelial cells in culture.

It has been postulated that in blood vessels under alpha(1)-related stimulation, the endothelial intracellular calcium concentration ([Ca(2+)](i)) increases, which is necessary to induce nitric oxide synthesis, is the result of an increase in vascular smooth muscle, which subsequently, flows into the endothelial cells through gap junctions and it is not the result of a direct adrenergic stimulation of endothelial receptors. Others, however, postulate that endothelial alpha(1D)-adrenoceptors, have a direct effect on nitric oxide synthesis. In order to clarify this phenomena, in this work we analyzed the presence of alpha(1)receptor subtypes and their functional association with nitric oxide synthesis in rat coronary microvascular endothelial cells in culture, with pharmacological, immunological and reverse transcriptase polymerase chain reaction approaches. Our results show the presence and functional coupling with nitric oxide synthesis of alpha(1A) and alpha(1D)-adrenoceptor subtypes. alpha(1B)-adrenoceptor subtype is not coupled with nitric oxide production.

Adrenergic alpha-Agonists↗
PubMed2006

Increases in tissue Pco2 during circulatory shock reflect selective decreases in capillary blood flow.

OBJECTIVES: Tissue Pco2 reflects metabolic alterations due to circulatory failure during circulatory shock. This study addresses simultaneous changes in gastric and buccal tissue Pco2 with changes in microcirculatory blood flow in a rat model of circulatory shock induced by cecal ligation and puncture. DESIGN: Prospective controlled laboratory study. SETTING: University-affiliated research laboratory. SUBJECTS: Male breeder Sprague-Dawley rats. INTERVENTIONS: Induction of polymicrobial, abdominal sepsis by cecal ligation and puncture. MEASUREMENTS AND MAIN RESULTS: Tissue Pco2 was continuously measured with the aid of a miniature carbon dioxide electrode. Using orthogonal polarization spectral imaging, recordings of the microcirculation were taken at baseline and hourly intervals until death and compared with sham-operated animals. Gastric and buccal tissue Pco2 values progressively increased in animals after cecal ligation and puncture and terminated in death. Microcirculatory blood flow in vessels >20 microm was well preserved during progression of shock, whereas there was an early and progressive decrease in microcirculatory blood flow in vessels <20 microm, mostly representing capillaries. Tissue Pco2, the tissue Pco2-Paco2 gradient, and blood flow in vessels <20 microm were highly correlated. This contrasted with sham control animals in which no significant hemodynamic, blood gas, lactate, microcirculatory, and tissue Pco2 abnormalities were observed. CONCLUSIONS: These observations suggest that microcirculatory failure in capillaries appears as an early defect in close association with anaerobic metabolism during progression of circulatory shock in an animal model of septic peritonitis.

Animals↗
PubMed2006

Comparison of buccal microcirculation between septic and hemorrhagic shock.

OBJECTIVE: Microcirculatory perfusion is disturbed in sepsis, and global hemodynamics does not necessarily reflect microcirculatory blood flow. In this study, we investigated the effect of the same level of mean arterial pressure (MAP) or cardiac index on the changes in buccal microcirculation between septic and hemorrhagic shock. DESIGN: Prospective, controlled laboratory study. SETTING: University-affiliated research laboratory. INTERVENTIONS: A total of 20 Sprague-Dawley rats were divided into four groups: 1) septic shock induced by cecal ligation and perforation: when MAP decreased to 80 mm Hg, saline was infused at a rate of 25 mL.kg.hr for 2 hrs; 2) both time- and MAP-matched hemorrhagic shock: approximately 30% of total blood volume was withdrawn during the corresponding interval, followed by infusion aiming to restore MAP as required when MAP decreased to 80 mm Hg; 3) both time- and cardiac index-matched hemorrhagic shock: approximately 40% of total blood volume was withdrawn during the corresponding interval until MAP decreased to 50 mm Hg, which generally generated a cardiac index similar to those in septic animals, followed by infusion at the same rate for 2 hrs; and 4) sham control: animals underwent the same procedure except no cecal ligation and perforation, bleeding, and infusion. MEASUREMENTS AND MAIN RESULTS: Buccal microcirculation was visualized with the aid of an orthogonal polarization spectral image device. A semiquantitative score was calculated for vessels of <20 mum, primarily representing the capillaries. Impaired buccal capillary blood flows in septic animals were more severe than those in MAP-matched hemorrhagic animals and were similar to those in cardiac index-matched hemorrhagic animals during the hypoperfusion period before infusion. Significantly improved global hemodynamics after resuscitation cannot effectively improve the buccal capillary blood flows in septic animals, in contrast to those in MAP-matched and cardiac index-matched hemorrhagic animals. CONCLUSIONS: Impaired microcirculatory alteration in septic shock is more severe than hemorrhagic shock; microcirculation is relatively independent of improved systemic hemodynamics, in contrast to those in hemorrhagic shock.

Animals↗
PubMed2006

Microcirculation during cardiac arrest and resuscitation.

OBJECTIVE: Direct observations of the microcirculation using orthogonal polarization spectral imaging have attracted attention and revealed that, especially in cardiogenic and distributive shock, there is discordance between the macrocirculation and the microcirculation. We evaluated serial changes and the effects of epinephrine on microcirculatory blood flow in the most severe form of circulatory failure, namely, cardiac arrest. DESIGN AND SETTING: : Controlled laboratory animal study. SUBJECTS AND INTERVENTIONS: A total of 15 pigs were subjected to 5 mins of ventricular fibrillation and 5 mins of precordial compression before electrical defibrillation was attempted. In a subset, six animals received 1 mg of epinephrine after 1 min of precordial compression. MEASUREMENTS AND MAIN RESULTS: Microcirculatory blood flow was visualized in the sublingual mucosa at baseline and 0.5, 1, and 5 mins of ventricular fibrillation, at 1 and 5 mins of precordial compression, and at 1 and 5 mins after return of spontaneous circulation. In addition, coronary perfusion pressure was recorded. Microcirculatory blood flow decreased dramatically in the 0.5 min after the onset of ventricular fibrillation. Precordial compression partially restored microcirculatory blood flow in each animal but to a significantly greater extent in animals that achieved return of spontaneous circulation. These changes were paralleled by similar changes in coronary perfusion pressure. Both variables were highly correlated. Administration of epinephrine resulted in a massive reduction of microcirculatory blood flow that lasted for >/=5 mins. CONCLUSIONS: In this model, microcirculatory blood flow was highly correlated with macrocirculatory hemodynamics, including coronary perfusion pressure in distinction with septic shock. Administration of epinephrine dramatically decreased microcirculatory blood flow.

Animals↗
PubMed2006

Evidence against alpha-adrenoceptors mediating relaxation in rat thoracic aortae: alpha-agonists relaxation depends on interaction with alpha-adrenoceptors.

In rat aorta, the presence of functional alpha(2)-adrenoceptors (alpha(2)-AR) was investigated in ring preparations preconstricted with alpha(1)-adrenergic and non- alpha(1)-adrenergic agonists. Particularly, the hypothetical interference of alpha(2)-AR agonists with alpha(1)-AR-mediated vasoconstriction was evaluated. Relaxant and contractile responses to alpha(2)-AR agonists were obtained. In endothelium-intact and endothelium-denuded aortic rings preconstricted with phenylephrine (1 x 10(-6) m), the imidazoline derivatives, clonidine and UK14304, induced relaxations with similar order of potencies (-log EC(50)) and maxima relaxant effects respectively. Pretreatment with the NO synthase inhibitor, N(G)-nitro-L-arginine methyl ester (L-NAME) had no effect on the relaxant responses to clonidine and UK14304. In phenylephrine-constricted rings with endothelium, relaxations to clonidine and UK 14304 were not antagonized by the selective alpha(2)-AR antagonist, rauwolscine (< or =1 x 10(-6) m). Clonidine and UK 14304 induced only contractions on endothelium-intact and endothelium-denuded aortic rings contracted with prostaglandin F(2alpha) (3 x 10(-7) m). Moreover, clonidine and UK 14304-induced relaxation of endothelium-denuded arteries precontracted with methoxamine but not with serotonin. Finally, the concentration-contraction curves to clonidine and UK 14304 in endothelium-denuded aortic rings were significantly shifted to the right by the alpha(1D)-AR selective antagonist, BMY 7378, and rauwolscine. The pA(2) and pK(B) values for BMY 7378 and rauwolscine, respectively, against endothelium-independent actions of clonidine and UK 14304 were characteristic of an effect on the alpha(1D)-AR. The other selective alpha(2)-AR agonist tested BHT 933 (an azepine derivative), lacks considerable relaxant and contractile effects in rat aorta. The results provide no evidence for the presence of functional alpha(2)-AR in rat aorta. Respectively, the relaxant and contractile effects of the imidazoline derivatives, clonidine and UK 14304, may be due to an adjustable (in relation to the agonist-dependent active state of the alpha(1)-AR), inhibitory and excitatory, interaction with alpha(1)-ARs.

Adrenergic alpha-Agonists↗
PubMed2005

Increases in both buccal and sublingual partial pressure of carbon dioxide reflect decreases of tissue blood flows in a porcine model during hemorrhagic shock.

BACKGROUND: Earlier studies had demonstrated that gastric partial pressure of carbon dioxide (PCO2) of the gastric wall is an early indication of perfusion failure. Because hypercarbia is a general phenomenon of perfusion failure, this study investigated whether sublingual and buccal mucosal tissue PCO2 also serve as a sensitive indicator of systemic blood flow during hemorrhagic shock. METHODS AND RESULTS: Hemorrhagic shock was induced in five male domestic pigs. Buccal and sublingual PCO2 increased from 60 to 129 mm Hg (p < 0.01) in parallel with average decreases in cardiac output to 44% (from 6.1 to 2.8 L/minute; p < 0.01), and mean arterial pressure to 47% (from 115 to 57 mm Hg; p < 0.01), over the 2-hour interval of shock. According to colored microspheres used for measurements, buccal mucosal flow decreased to 35% (from 6.3 to 2.2 mL/minute/100 g; p < 0.01) in close parallel with sublingual blood flow, which decreased to 34% (from 7.2 to 2.5 mL/minute/100 g; p < 0.01). Liver flow decreased to 56% (from 152 to 85 mL/minute/100 g;p < 0.01), and renal flow to 47% (from 272 to 128 mL/minute/100 g;p < 0.01) of baseline values. The procedure yielded to overall comparable volume exchanges in different animals. After reinfusion of shed blood, buccal PCO2, like sublingual PCO2, was restored to approximately baseline values (respectively, from 56 to 71 mm Hg and from 60 to 71 mm Hg; p = not significant), together with arterial pressure, cardiac output, and end-tidal CO2 (EtCO2) (respectively, from 115 to 115 mm Hg, from 6.1 to 6.3 L/minute, and from 35 to 39 mm Hg; p = not significant), but there was delayed reversal of lactic acidosis (from 0.7 to 2.5 mmol/L;p < 0.01). In five unbled control animals, no significant changes were observed over the same interval. CONCLUSION: The current study extends the rationale for noninvasive measurements to both buccal and sublingual mucosa for diagnosis and quantitation of hemorrhagic shock severity.

Animals↗
PubMed2004

Miniaturized chest compressor.

BACKGROUND: Current American Heart Association guidelines call for continuous manual chest compressions for cardiopulmonary resuscitation. Chest compressions maintain critical levels of forward blood flow, including blood flow to the myocardium during cardiac arrest, to allow for successful resuscitation. The demand on rescuers is to ensure that compression is consistent, with appropriate force and depth, often under difficult conditions of rescue, evacuation, and transport. It is also of great moment that fatigue of the rescuer adversely affects outcomes. This evaluation was to compare two pneumatically driven devices, the Michigan Thumper (Michigan Instruments, Grand Rapids, MI), as an industrial standard, and the miniaturized chest compressor. METHODS: On a porcine model of cardiopulmonary resuscitation, alternating current fibrillation was induced for 7 mins, followed by 5 mins of chest compression. Arterial and right atrial pressures and end-tidal CO2 were measured. Coronary perfusion pressure was calculated as the difference between compression end-diastolic arterial pressure and right atrial pressure. RESULTS: Threshold levels of coronary perfusion pressure (>15 mm Hg) and end-tidal CO2 (>10 mm Hg) for successful defibrillation were maintained with the miniaturized chest compressor. Consistently greater coronary perfusion pressure and end-tidal CO2 values were achieved with the miniaturized chest compressor in comparison with the Thumper. CONCLUSION: The miniaturized chest compressor has the important potential advantage of minimal weight and, therefore, portability, without any reduction in effectiveness. To the contrary, it is potentially more effective than the much larger and heavier industry standard for maintaining circulation.

Animals↗
PubMed2004

Impairment of smooth muscle function of rat thoracic aorta in an endothelium-independent manner by long-term administration of N(G)-nitro-L-arginine methyl ester.

In this study, we aimed to elucidate whether the daily hypertensive dose of long-term N(G)-nitro-l-arginine methyl ester (l-NAME) treatment, could make a difference between endothelial and smooth muscle functions in rat thoracic aorta. We test the hypothesis that high-dose, long-term l-NAME treatment has a depressive effect on vascular smooth muscle contractile activity which is not related with nitric oxide (NO) synthesis inhibition. After 14 days of treatment, isometric tension and (45)Ca(2+) influx were measured in aortic tissues isolated from l-NAME(10) and l-NAME(100) hypertensive (10 and 100 mg/kg/day, systolic blood pressures 167 +/- 7 and 172 +/- 10 mmHg, respectively) and control normotensive rats (132 +/- 7 mmHg). In l-NAME(10)- and l-NAME(100)-treated rats, acetylcholine-induced relaxation in aortic rings was suppressed with no significant difference between the treatments. l-NAME(100) (but not l-NAME(10)) treatment, significantly inhibited contractile responses to phenylephrine, angiotensin II, and K(+) (80 mm) in endothelium-intact tissues. The effect of l-NAME(100) on phenylephrine-induced contractile responses was not observed after 3 days of treatment. In endothelium-denuded aortic tissues of l-NAME(100) (but not l-NAME(10))-treated rats, phenylephrine (1 x 10(-6) m)- and K(+) (80 mm)-induced contractions and (45)Ca(2+) influxes were significantly reduced. In Ca(2+)-free medium (0.1 mm EDTA), on the contrary, the transient contractions obtained by either phenylephrine (1 x 10(-6) m) or caffeine (1 x 10(-2) m), or the sustained contractions induced by 12-o-tetradecanoylphorbol-13-acetate (1 x 10(-6) m; a protein kinase C activator) in endothelium-denuded aortic rings, were not modified by both l-NAME treatments. These results indicate that in aortic rings from l-NAME hypertensive rats, low and high doses, long-term l-NAME administration may be associated with equivalent inhibition in NO-dependent vasodilator tone (corresponding to equivalent hypertension values); whereas only high-dose, long-term l-NAME administration produces an endothelium-independent decrease in vasocontrictor activity, at least partly explained by a reduction in extracellular Ca(2+) influx.

Adrenergic alpha-Agonists↗
PubMed2003

Purification of gastroprotective triterpenoids from the stem bark of Amphipterygium adstringens; role of prostaglandins, sulfhydryls, nitric oxide and capsaicin-sensitive neurons.

In this investigation three bioactive compounds, responsible for the gastroprotective property of Amphipterygium adstringens, were purified from an active dichloromethane fraction. These compounds were 3alpha-hydroxymasticadienonic acid, beta-sitosterol and 3- epi-oleanolic acid. The latter was the most active compound (88.8 % of gastroprotection) followed by 3alpha-hydroxymasticadienoic acid and beta-sitosterol (69.8 and 42.5 % of gastroprotection, respectively). Carbenoxolone was used as positive control and it showed 88.4 % of gastroprotection. Masticadienonic acid was also isolated from the active fraction, but it was unable to inhibit the ethanol-induced gastric lesions. The gastroprotection of the methanol extract was completely inhibited by the pretreatment with l-NAME and attenuated by pretreatment with indomethacin and N-ethylmaleimide. These results suggest that endogenous nitric oxide plays an important role in the gastroprotection of A. adstringens methanol extract on ethanol-induced gastric mucosal lesions and that there is partial participation by prostaglandins and endogenous sulfhydryls. The effect of 3alpha-hydroxymasticadienonic acid was attenuated only by pretreatment with N-ethylmaleimide, indicating that endogenous sulfhydryls (thiols) participate in its gastroprotective mechanism. Capsaicin-sensitive afferent neurons do not participate in the gastroprotection of either the methanol extract or 3alpha-hydroxymasticadienoic acid.

Animals↗
PubMed2003

Lipid requirements of infants: implications for nutrient composition of fortified complementary foods.

Dietary lipids have traditionally been considered as solely part of the exchangeable energy supply. The main consideration in infant nutrition has been the amount of fat that can be tolerated and digested by infants and young children. The significance of the composition of dietary fat has received little attention. Presently, there is a growing interest in the quality of dietary lipid supply in early childhood as a major determinant of growth, infant development and long-term health. Thus, the selection of dietary lipids during the first years of life is now considered to be critically important for health and good nutrition throughout the life course. Over the past decades interest has focused on the role of essential lipids in central nervous system development and of fatty acids and cholesterol in lipoprotein metabolism throughout life. Lipids are structural components of all tissues and are indispensable for cell and plasma membrane synthesis. The brain, retina and other neural tissues are particularly rich in long-chain PUFA. Some (n-6) and (n-3) fatty acids are precursors for eicosanoid formation; these are powerful mediators of numerous cell and tissue functions. Recommendations for infant nutrition and implications of these for the nutrient composition of complementary foods are presented and discussed. There is more to fat than its role as a key fuel in energy metabolism and body energy storage; lipids are essential for tissue growth, cardiovascular health, brain development and function throughout the life course.

Absorption↗
PubMed2003

Acute lead exposure induces renal haeme oxygenase-1 and decreases urinary Na+ excretion.

The effects of acute lead exposure on renal function, lipid peroxidation and the expression of haeme oxygenase (HO) in rat kidney were determined. A single injection of lead acetate (50 mg Pb/kg) was given to rats. Changes in renal function, characterized by a significant reduction in the Na+ excretion was observed six hours after Pb exposure; this effect persisted for 24 hours. TBARS levels increased in kidney cortex 24 hours after Pb administration. In kidney cortex, Pb exposure affected the expression of HO-1, a renal protein associated with oxidative stress. HO-1 mRNA increased 2.3-fold, three hours after Pb administration and remained increased for six, 12 and 24 hours. HO enzymatic activity and HO-1 protein increased six and three hours after Pb administration, respectively, and remained increased at 24 hours. HO inhibition by tin-protoporphyrin, potentiated Pb-induced increase in TBARS and prevented the Pb-induced reduction in Na+ excretion. Our data suggest that Pb may be acting through the generation of oxidant products and induction of HO.

Gene Expression↗
PubMed2002

Does segmental difference in alpha 1-adrenoceptor subtype explain contractile difference in rat abdominal and thoracic aortae?

The cyclooxygenase inhibitor, indomethacin, depresses adrenergic agonist constriction of endothelium-denuded rat abdominal, but not thoracic, aorta. In order to explain this finding, we explored the possibility of segmental differences in the population of alpha 1-adrenoceptor (AR) subtypes. In endothelium-denuded tissues, phenylephrine elicited concentration-dependent contractions in the thoracic and abdominal aortic rings with potencies and maximal effects that, respectively, did not differ significantly (P > .05). Indomethacin (1 x 10(-5) M) inhibited phenylephrine-induced contractions only in abdominal aorta. The subtype-selective alpha 1D-AR antagonist, BMY 7378, was found to antagonize contractions to phenylephrine competitively in abdominal (pA2 8.44) and thoracic (pA2 8.56) aortic rings. These data are consistent with published alpha 1D-AR functional potency and clonal alpha 1D-AR binding affinity. In addition, cumulative concentration-contraction curves for phenylephrine were competitively antagonized in the rat abdominal and thoracic aortae by prazosin, 5-methylurapidil and WB 4101, with pA2 values of 9.39 and 9.61, 7.64 and 7.85, and 9.43 and 9.58, respectively. These compounds with varying degrees of subtype selectivity inhibited contractions of the thoracic and abdominal aortae with affinities consistent with those determined at the alpha 1D-AR subtype. The results of this study suggest that the contraction to phenylephrine of the rat abdominal and thoracic aorta is mediated via the same alpha 1D-AR subtype.

Adrenergic alpha-Agonists↗
PubMedDate not supplied

[Testosterone inhibits the contractile responses to phenylephrine associated with the release of intracellular calcium in rat aorta].

Using endothelium-denuded rat aortic rings incubated in Ca2+ -free solution, we assessed the ability of testosterone to influence the contractile effect of phenylephrine, and the increase in resting tone (IRT) associated with Ca2+ ability to cross the plasma membrane. The addition of testosterone [10(-5)-10(-4) 5 min before phenylephrine [10(-6) M], inhibited both phenylephrine-induced contraction and IRT. These changes were not affected by cycloheximide (10(-5) M; a protein synthesis inhibitor of), flutamide (10(-5) M; an androgenic receptor antagonist), or by adding aminoglutethimide (10(-5) M; an aromatase inhibitor). Testosterone also blocked the contractile response to serotonin [10(-5) M] but not to caffeine [10(-2) M]. On the other hand, testosterone inhibited the contractile responses to cyclopiazonic acid (10(-6) M; a selective Ca2+ -ATPase inhibitor) or ryanodine (10(-5 M; an activator of sarcoplasmic reticulum Ca2+ -release channels) associated with capacitative Ca2+ influx through non-L-type Ca2+ channels. These data suggest that by acting on the cellular membrane, testosterone interferes with the signal transduction pathway of G(q-11) protein-coupled receptors, and inhibits capacitative Ca2+ influx through both L-type and non-L-type Ca2+ channels. These effects are non-genomic, non-mediated by the intracellular androgen receptor, and not due to the conversion of testosterone to estrogens.

Animals↗