Adrenergic mechanisms in canine nasal venous systems.

1 We investigated the adrenergic mechanisms of the two venous systems that drain the nasal mucosa, thereby their exact role in eliciting nasal decongestion. The action of endogenously released noradrenaline and exogenous adrenergic agonists on different segments of the nasal venous systems, i.e. collecting (LCV, SCV) and outflow (SPV) veins of posterior venous system, collecting (ACV) and outflow (DNV) veins of anterior venous system and venous sinusoids of the septal mucosa (SM), were studied. In vitro isometric tension of the vascular segments was measured. 2 Transmural nerve stimulation (TNS) produced constriction in ACV, DNV and SM, primary constriction followed by secondary dilatation in LCV and SCV and dilatation in SPV. Tetrodotoxin (10(-6) M) abolished all responses. Phentolamine (10(-6) M), prazosin (10(-6) M) and rauwolscine (10(-7) M) inhibited the constriction in all venous vessels. Propranolol (10(-6) M), atenolol (10(-6) M) and ICI 118,551 (10(-6) M) inhibited the relaxation in SPV but not in LCV and SCV. Phenylephrine and clonidine constricted whereas dobutamine and terbutaline relaxed all venous vessels dose-dependently. 3 These results indicate alpha(1)-, alpha(2)-, beta(1)- and beta(2)-adrenoceptors are present in both venous systems. TNS causes constriction of anterior venous system, venous sinusoids and posterior collecting veins primarily via postjunctional alpha(2)-adrenoceptors but relaxation of posterior outflow vein equally via postjunctional beta(1)- and beta(2)-adrenoceptors. The combined action of the two adrenergic mechanisms can reduce nasal airway resistance in vivo by decreasing vascular capacitance and enhancing venous drainage via the posterior venous system.

Morphometric study on leydig cells in capsulotomized testis of rats.

AIM: To further clarify the changes occurred in the testicular capsulotomized rats. METHODS: In testicular capsulotomized and sham-operated rats, the cross sectional area, the nucleus diameter and the number of Leydig cells were morphologically analyzed by the Vidas Image Processing System connected to a microscope. RESULTS: In the capsulotomized animals, the cross sectional area of Leydig cells was gradually increased from 30 days onwards. There was no obvious change in the nucleus diameter of Leydig cells. However, The Leydig cell number was significantly increased from day 30 onwards. CONCLUSION: In rats, testicular capsulotomy may induce hyperplasia/hypertrophy of Leydig cells in the testis.

M1 and M3 muscarinic receptors mediate relaxation and contraction in canine nasal veins.

BACKGROUND: Acetylcholine (ACh) has been shown to induce nasal congestion via vasorelaxation of intranasal posterior collecting veins (PCV) coupled with vasocontraction of extranasal outflow veins (dorsal nasal vein [DNV] and sphenopalatine vein [SPV]). The aim of this study was to characterize the muscarinic receptor subtype(s) involved in ACh-induced relaxation and contraction in canine nasal veins. METHODS: PCV, DNV, and SPV were isolated from the canine nose. In vitro isometric tension of segments from these veins was monitored to reflect vascular reactivity. ACh concentration-response curve was studied in the presence of muscarinic receptor subtype inhibitors. Immunohistochemical localization of M(1)-M(5) receptor subtypes in the veins was performed. RESULTS: ACh-induced relaxation in PVC was inhibited by pertussis toxin (PTX; inhibitor of G-protein that couples M(2)/M(4) receptors), methoctramine (selective M(2) muscarinic receptor inhibitor), muscarinic toxin 7 (MT-7; selective M(1) muscarinic receptor inhibitor), and 4-diphenylacetoxy-methylpiperidine methiodide (4-DAMP; selective M(3) muscarinic receptor inhibitor). ACh-induced contraction in SPV and DNV was potentiated by PTX and methoctramine but was inhibited by MT-7 and 4-DAMP. Immunohistochemistry confirmed the presence of five muscarinic receptor subtypes in the endothelium of nasal veins, with staining of M(3) > M(1) > M(5) > M(2) = M(4) in PVC but M(2) = M(4) > M(3) > M(1) > M(5) in outflow veins. M(1) and M(3) receptor subtypes were localized in the smooth muscles of both types of veins. CONCLUSION: The results show that ACh relaxes intranasal veins and contracts extranasal veins primarily via M(1) and M(3) muscarinic receptor subtypes, implying the therapeutic value of M(1)/M(3)-specific or highly selective anticholinergics on nasal congestion.

Autonomic nervous control of myoepithelial cells and secretion in submandibular gland of anaesthetized dogs.

In dog submandibular gland, the activity of myoepithelial cells was assessed by simultaneous measurement of intraductal pressure (P(du)) and subcapsular pressure (P(ca)) using catheter-tip pressure transducers; their resting values were 2.5 +/- 0.21 and 3.0 +/- 0.19 mmHg, respectively (n = 40). Retrograde infusion of saliva (collected from preceding parasympathetic nerve stimulation) increased P(du) (coefficient of 50 mmHg ml(-1) for rates < 1 ml min(-1) and 85 mmHg ml(-1) for higher rates) and P(ca) (coefficient of 0.47 mmHg ml(-1) for all rates). Blood flow changes did not affect P(du) but increased P(ca) (coefficient of 0.04 mmHg ml(-1)). Parasympathetic nerve stimulation increased P(du) but decreased P(ca) abruptly; the response threshold was 0.1 Hz, with maximal responses at 16 Hz. The coefficients for P(du) and P(ca) on salivary secretion to parasympathetic nerve stimulation in glands with spontaneous blood flow (5.3 x 10(-3) and 4.87 x 10(-2) ml min(-1) g(-1) mmHg(-1)) were close to their values in glands with constant-flow vascular perfusion (4.9 x 10(-3) and 3.68 x 10(-2) ml min(-1) g(-1) mmHg(-1)). The finding that P(ca) fell despite concomitant increased blood flow suggests contraction of myoepithelial cells. Additional ductal occlusion further increased P(du) and enhanced the fall in P(ca), suggesting that the myoepithelial cells can contract when distended. Atropine blocked salivary secretion and responses of P(du) and P(ca) to parasympathetic nerve stimulation. ACh elicited responses similar to that of parasympathetic nerve stimulation. VIP caused very scanty salivary secretion and gradual slight increases in P(du) and P(ca); the change in P(ca) was abolished in glands with constant-flow vascular perfusion. Hence, contraction of myoepithelial cells to parasympathetic nerve stimulation is via muscarinic receptors. Sympathetic nerve stimulation increased P(du) and decreased P(ca) abruptly; the response threshold was 0.1 Hz, with maximal responses at 16 Hz. The coefficients for P(du) and P(ca) on salivary secretion to sympathetic nerve stimulation in glands with spontaneous blood flow (3.0 x 10(-3) and 3.2 x 10(-3) ml min(-1) g(-1) mmHg(-1)) were similar to their values in glands with constant-flow vascular perfusion (3.2 x 10(-3) and 3.1 x 10(-3) ml min(-1) g(-1) mmHg(-1)). The finding that P(ca) fell even in glands with constant-flow vascular perfusion suggests contraction of myoepithelial cells. Superimposed sympathetic nerve stimulation immediately enhanced the pressure changes and secretory response to parasympathetic nerve stimulation, indicating that the two autonomic nerves act synergistically to evoke myoepithelial cell contraction. Phentolamine and prazosin but not propranolol and yohimbine blocked the sympathetic enhancement. The finding that phenylephrine, but not clonidine and isoproterenol, abruptly decreased P(ca) in glands with constant-flow vascular perfusion suggests that the sympathetic activation of myoepithelial cells is via the alpha(1)-adrenoceptors.