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Background/aims: A previous study has demonstrated that endogenous male sex hormones do not alter neuronal nitric oxide (NO) release in rat mesenteric artery. However, the regulatory role of endogenous male sex hormones on noradrenaline (NA) release in rat mesenteric artery is not known. The present study was designed to analyze whether endogenous male sex hormones influence the NA release induced by electrical field stimulation (EFS), as well as the possible modification in NA and neuronal NO release by presynaptic beta-adrenoceptor activation. Methods: For this purpose, mesenteric arteries from control and orchidectomized male Sprague-Dawley rats were used. Basal and EFS-induced neuronal NO and NA release, as well as the contractile effect induced by EFS, was measured. Results: Basal and EFS-induced neuronal NO and NA release were similar in arteries from control and orchidectomized rats. The beta-adrenoceptor agonist clenbuterol did not modify EFS-induced neuronal NO and NA release in arteries from control rats. In contrast, in arteries from orchidectomized animals, clenbuterol increased both neuronal NO and NA release; this increase was prevented by incubation with the beta-adrenoceptor antagonist propranolol. However, the contractile response elicited by EFS was not modified by clenbuterol in either group of rats. Conclusions: These results show that orchidectomy does not alter the EFS-induced NA release. What is more, activation of presynaptic beta-adrenoceptors does not modify EFS-induced NA and neuronal NO release in arteries from control rats although it increases the release of both neurotransmitters in arteries from orchidectomized rats. Despite these modifications, the EFS-induced contractile response is preserved in arteries from orchidectomized rats., Depto. de Biología Celular, Fac. de Odontología, TRUE, pub

Objectives To investigate whether hypertension could modify the function of adrenergic, nitrergic, and sensory innervations involved in the electrical field stimulation-induced response in mesenteric arteries from female rats. Methods Vascular reactivity experiments were performed in endothelium-denuded mesenteric arteries from normotensive, Wistar–Kyoto and spontaneously hypertensive female rats; protein expression was measured by western blot; nitric oxide release was measured by fluorometry; calcitonin gene-related peptide and noradrenaline release were determined by enzyme immunoassay. Results The electrical field stimulation-induced contractions were significantly lower in segments from spontaneously hypertensive rats than those of Wistar–Kyoto rats. Hypertension did not modify either the response or release of noradrenaline. Preincubation with the nitric oxide synthase inhibitor NG-nitro-L-arginine methyl ester increased the electrical field stimulation-induced contractions only in segments from Wistar–Kyoto rats. The relaxation induced by the nitric oxide donor sodium nitroprusside was similar in segments from both strains. The electrical field stimulation-induced nitric oxide release was decreased in segments from spontaneously hypertensive rats. The calcitonin gene-related peptide receptor antagonist CGRP(8–37) did not alter the electrical field stimulation-induced contractions in segments from Wistar–Kyoto rats but increased them in segments from spontaneously hypertensive rats. The calcitonin gene-related peptide-induced relaxation was increased in segments from spontaneously hypertensive rats. The expression of the 15-kDa active form of RAMP1 was increased in segments from spontaneously hypertensive rats. Conclusion In contrast to male rats, electrical field stimulation-induced contractions are decreased in hypertensive female rats. Nitrergic innervation plays a role in the development and/or maintenance of hypertension, whereas sensory innervation is a, Direccion General de Ciencia y Tecnologia, Instituto de Salud Carlos III Spanish Government, Depto. de Biología Celular, Fac. de Odontología, TRUE, pub

The aim of this study was to analyze whether endogenous male sex hormones influence the release of thromboxane A2(TXA2) and its role in the electrical field stimulation (EFS)-induced response, as well as the mechanism involved. For this purpose, endothelium-denuded mesenteric arteries from control and orchidectomized male Sprague-Dawley rats were used to measure TXA2 release; EFS-induced response, nitric oxide (NO), norepinephrine (NA), and prostaglandin (PG) I2 release were also measured in the presence of the TXA2 synthesis inhibitor furegrelate. Orchidectomy increased basal and EFS-induced TXA2 release. Furegrelate decreased the EFS-induced contraction in arteries from control rats, but did not modify it in arteries from orchidectomized rats. The EFS-induced neuronal NO release and vasodilator response were increased by furegrelate in arteries from control rats, but were not modified in arteries from orchidectomized rats. Furegrelate did not modify the EFS-induced NA release or vasoconstrictor response in arteries from either control or orchidectomized rats. The EFS-induced PGI2 release was not modified by furegrelate in arteries from control rats, but was increased in arteries from orchidectomized rats. The results of the present study show that endogenous male sex hormone deprivation i) increases non-endothelial TXA2 release and ii) regulates the effect of endogenous TXA2 on the EFS-induced response through different mechanisms that, at the least, involve the NO and PGI2 systems. In arteries from control rats, inhibition of TXA2 formation decreases the EFS-induced response by increasing neuronal NO release. In arteries from orchidectomized rats, the EFS-induced response is unaltered after the inhibition of TXA2 formation, by increasing PGI2 release., Fondo de Investigaciones Sanitarias, Fundación de Investigación Médica Mutua Madrileña, Depto. de Biología Celular, Fac. de Odontología, TRUE, pub

Our study determines alterations in the vasoconstrictor response elicited by electric field stimulation (EFS) in mesenteric arteries from cirrhotic rats treated with CCl(4), and how calcitonin gene-related peptide (CGRP) participates in this response. Vasoconstriction induced by EFS was analysed in the absence and presence of the CGRP receptor antagonist CGRP(8-37) in arterial segments from control and cirrhotic rats. The vasodilator response to exogenous CGRP was tested in both groups of rats, and the interference of the guanylate cyclase inhibitor ODQ or the K(ATP) channel blocker glibenclamide was analysed only in segments from cirrhotic rats. The vasodilator response to the K(ATP) channel opener pinacidil and to 8-bromo-cyclic GMP was tested. The K(ATP) currents were recorded using the patch-clamp technique. Expression of receptor activity-modifying protein 1 (RAMP1), calcitonin receptor-like receptor, Kir 6.1 and sulfonylurea receptor 2B (SUR2B) was also analysed. Release of CGRP and cGMP was measured. The EFS-elicited vasoconstriction was less in segments from cirrhotic rats. The presence of CGRP(8-37) increased the EFS-induced response only in segments from cirrhotic rats. The CGRP-induced vasodilatation was greater in segments from cirrhotic rats, and was inhibited by ODQ or glibenclamide. Both pinacidil and 8-bromo-cyclic GMP induced a stronger vasodilator response in segments from cirrhotic rats. Pinacidil induced greater K(ATP) currents in cirrhotic myocytes. Expression of RAMP1, calcitonin receptor-like receptor, Kir 6.1 and SUR2B was not modified by liver cirrhosis. Liver cirrhosis increased CGRP release, but did not modify cGMP formation. The decreased vasoconstrictor response to EFS in cirrhosis is mediated by increased vasodilator response to CGRP, as well as increased K(ATP) channel gating. This effect of CGRP may play a role in the splanchnic vasodilatation present in liver cirrhosis., Instituto de Salud Carlos III Spanish Government DEP2006-56187-C04-04, Ministerio de Ciencia e Innovación (SAF09-10374), Depto. de Biología Celular, Fac. de Odontología, TRUE, pub

Background and purpose: The present study was designed to assess whether cyclooxygenase-2 (COX-2) activation is involved in the effects of chronic aldosterone treatment on endothelial function of mesenteric resistance arteries (MRA) from Wistar-Kyoto (WKY) and spontaneously hypertensive rats (SHR). Experimental approach: Relaxation to acetylcholine was measured in MRA from both untreated and aldosterone-treated strains. Vasomotor responses to prostacyclin and U46619 were also analysed. Release of 6-oxo-prostaglandin (PG)F1alpha and thromboxane B2 (TxB2) was determined by enzyme immunoassay. COX-2 protein expression was measured by western blot. Key results: Aldosterone reduced acetylcholine relaxation in MRA from both strains. In MRA from both aldosterone-treated strains the COX-1/2 or COX-2 inhibitor (indomethacin and NS-398, respectively), TxA2 synthesis inhibitor (furegrelate), prostacyclin synthesis inhibitor (tranylcypromine) or TxA2/ PGH2 receptor antagonist (SQ 29 548), but not COX-1 inhibitor SC-560, increased acetylcholine relaxation. In untreated rats this response was increased only in SHR. Prostacyclin elicited a biphasic vasomotor response: lower concentrations elicited relaxation, whereas higher concentrations elicited contraction that was reduced by SQ 29 548. Aldosterone increased the acetylcholine-stimulated production of 6-oxo-PGF(1alpha) and TxB2 in MRA from both strains. COX-2 expression was higher in both strains of rats treated with aldosterone. Conclusions and implications: Chronic treatment with aldosterone impaired endothelial function in MRA under normotensive and hypertensive conditions by increasing COX-2-derived prostacyclin and thromboxane A2. As endothelial dysfunction participates in the pathogenesis of many cardiovascular disorders we hypothesize that anti-inflammatory drugs, specifically COX-2 inhibitors, could ameliorate vascular damage in patients with elevated aldosterone production., Fondo de Investigaciones Sanitarias (PI051767), Comisión de Ciencia y Tecnología (SAF-2006-07888), Banco de Santander-UAM, Depto. de Biología Celular, Fac. de Odontología, TRUE, pub

Cell biology and histology are basic sciences that study the levels of organization between the gross morphological and the molecular levels. They are included in the curricula of the preclinical years of medical and dental degrees. Cell biology and histology courses are usually perceived as difficult to pass and high failure rates reduce indeed learners’ interest and engagement. Research has shown that students learn more while actively engaged, and that engagement occurs through interactions with the content, peers, and instructors. Among active learning strategies, an adaptive flipped classroom (AFC) is an advanced approach based on interactions between instructors and students prior to face-to-face sessions. Learners are expected to complete some assignments meant to make them reflect and reveal their comprehension and learning difficulties. With this methodology, instructors can tailor teaching to their specific needs. A pilot AFC approach was implemented in the Cell Biology and Histology subject which is part of the Dental Degree at the Complutense University of Madrid. AFC was applied to 42% of the histology syllabus along two consecutive courses. At the beginning of the 2021-22 course, the class was split into two halves due to the pandemic, so while one-half of the students went to face-to-face classes the other half attended online via Microsoft Teams. The two halves turned weekly, so all the students attended the same number of face-to-face and online sessions. As a result of the improvement of the pandemic, two months after the beginning, classes reverted to conventional face-to-face teaching just after finishing AFC units. The aim of the present study is to present an AFC approach applied to the histology program of a dentistry degree to enhance engagement and active learning, the student’s perceptions, and to assess if appraisals were consistent or not in two consecutive courses. A high level of engagement was achieved in both courses, the materials pr