scholarly journals Phenylephrine induces relaxation of longitudinal strips from small arteries of goat legs

2019 ◽  
Author(s):  
Kawin Padmaja Marconi ◽  
Bhavithra Megan ◽  
Alen Major Venis ◽  
Renu Raj ◽  
Sathya Subramani
Keyword(s):  
Smooth Muscle ◽  
Adrenergic Receptor ◽  
Contractile Response ◽  
Receptor Subtype ◽  
Adrenergic Stimulation ◽  
Small Artery ◽  
Small Arteries ◽  
Alpha Adrenergic Receptor ◽  
Longitudinal Smooth Muscle ◽  
Relaxant Response

AbstractAlpha adrenergic stimulation is known to produce vasoconstriction. We have earlier shown that, in spiral strips of small arteries Phenylephrine (PE) caused vasorelaxation under high nitric oxide (NO) environment. However on further experimentation it was realized that the PE-induced vasorelaxant response occurred only with longitudinal strips of small arteries even under normal NO environment while circular strips showed contraction with PE even under high NO environment. Such PE-induced vasorelaxation of longitudinal strips was blocked by Phentolamine, an alpha-adrenergic receptor blocker. On delineation of specific receptor subtype, PE-induced relaxation was found to be mediated through alpha 1D receptor. However, this phenomenon is specific to small artery, as longitudinal smooth muscle of aorta showed only contractile response to adrenergic stimulation. There is no prior report of longitudinal smooth muscle in small artery up to our knowledge. The results of this study and histological examination of vessel sections suggest the presence of longitudinal smooth muscle in small artery and their relaxant response to alpha adrenergic stimulation is a novel phenomenon.

scholarly journals Alpha1‐adrenergic receptor subtype specific activation of ERK in human primary smooth muscle cells (1065.4)

2014 ◽  
Vol 28 (S1) ◽  
Author(s):  
Kaitlyn Brown ◽  
Timothy Aungst ◽  
Christian Castro ◽  
Ajay Bommareddy ◽  
Adam VanWert ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Adrenergic Receptor ◽  
Muscle Cells ◽  
Receptor Subtype

Muscarinic and alpha-adrenergic stimulation of Na and Ca uptake by dispersed lacrimal cells

1980 ◽  
Vol 239 (2) ◽  
pp. G99-G105 ◽  
Author(s):  
R. J. Parod ◽  
B. A. Leslie ◽  
J. W. Putney
Keyword(s):  
Lacrimal Gland ◽  
Adrenergic Receptor ◽  
Receptor Activation ◽  
Adrenergic Stimulation ◽  
Alpha Adrenergic Receptor ◽  
Ca Uptake ◽  
Isotope Technique ◽  
Ca Ions ◽  
Double Isotope

Rat lacrimal gland acinar cells were isolated and observed to be physiologically stable for several hours of incubation in vitro. With a double-isotope technique, it was found that carbachol and epinephrine stimulated the uptake of 22Na and 45Ca by lacrimal cells. These respnses were maximal at agonist concentrations of 10(-5) M and were blocked by atropine and phentolamine, respectively. It is concluded that muscarinic and alpha-adrenergic receptor activation increase the membrane permeability of the lacrimal gland acinar cell to Na and Ca, ions that may be important in the secretion of water by the lacrimal gland.

Effect of antihypertensive treatment on small artery remodeling in hypertension

2003 ◽  
Vol 81 (2) ◽  
pp. 168-176 ◽  
Author(s):  
Ernesto L Schiffrin
Keyword(s):  
Smooth Muscle ◽  
Enzyme Inhibitors ◽  
Beta Blockers ◽  
Angiotensin Converting Enzyme Inhibitors ◽  
Channel Blockers ◽  
Converting Enzyme ◽  
Small Artery ◽  
Converting Enzyme Inhibitors ◽  
Hypertensive Patients ◽  
Small Arteries

Blood vessels are remodeled in hypertension both structurally and functionally. The changes that occur in their structure, mechanical properties, and function contribute to blood pressure elevation and to complications of hypertension. We studied the remodeling of small arteries in experimental animals and humans. Smooth muscle cells of small arteries are restructured around a smaller lumen, with significant remodeling of the extracellular matrix and collagen and fibronectin deposition. Interestingly, there is no evidence of net growth of the vascular wall (which results in so-called eutrophic remodeling), particularly in the milder forms of human essential hypertension. Hypertrophic remodeling and increased small artery stiffness may be found in more severe forms of hypertension. Almost all hypertensive patients have vascular structural remodeling. However, only some exhibit endothelial dysfunction. This is particularly true in mild hypertension, in which endothelial dysfunction is less common. A 1-year treatment of hypertensive patients with angiotensin converting enzyme inhibitors, angiotensin AT1 receptor antagonists, and long acting calcium channel blockers corrected small artery structure and, to variable degrees depending on the agents used, impaired endothelial function. In contrast, beta blockers did not improve structure, function, or mechanics of vessels. When beta-blocker-treated patients were switched to an AT1 receptor antagonist, small artery structure and impaired endothelial function were corrected. The vascular protective action of some antihypertensive agents may contribute to improve outcome for hypertensive patients, although this is presently unproven.Key words: resistance arteries, smooth muscle, hypertrophy, endothelium, angiotensin converting enzyme inhibitors, AT1 receptor antagonists, calcium channel blockers, beta blockers.

Contraction of arterial smooth muscle induced by magnesium ions

1982 ◽  
Vol 242 (1) ◽  
pp. C25-C30 ◽  
Author(s):  
T. Ohhashi ◽  
T. Azuma
Keyword(s):  
Smooth Muscle ◽  
Dose Response ◽  
Contractile Response ◽  
Smooth Muscles ◽  
Bathing Solution ◽  
Magnesium Ions ◽  
Arterial Smooth Muscle ◽  
Relaxant Response ◽  
Per Se ◽  
Dose Dependent

Dose-response relationships for Mg2+ in a Mg2+-free bathing solution were obtained with isolated canine femoral arteries. At concentrations less than 5 mM, relaxant responses appeared in the preparations. In a concentration range of 10-20 mM, however, every one of the preparations invariably showed dose-dependent contractions. The relaxant and contractile responses were induced by the action of Mg2+ per se but not by the hyperosmolarity associated with the addition of Mg2+. Neither response was affected by the drugs that inhibited the actions of catecholamine, acetylcholine, serotonin, or histamine. The contractile response was kept unchanged in Ca2+-free Locke's solution and was almost independent of environmental calcium concentrations ranging from 2.2 to 8.2 mM. The contractile response was not affected under the influence of Ca antagonists, verapamil, or Mn2+. The presence of Ba2+ or Sr2+ enhanced the relaxant response and dose dependently suppressed the contractile response. The contractile response was still evoked in smooth muscles that were in the state of K+ contracture. These results suggest the possibility that the contractile action of Mg2+ was mediated by a release of intracellular Ca2+ or exerted directly on the contractile machinery of arterial smooth muscle.

Simo Decoction Stimulates Contractions of Antral Longitudinal Smooth Muscle via Multitudinous Mechanisms

2012 ◽  
Vol 18 (2) ◽  
pp. 113-120 ◽  
Author(s):  
Chibing Dai ◽  
Wei Qian ◽  
Na Liu ◽  
Jing Gong ◽  
Wenmei Chen ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Smooth Muscle ◽  
Nicotinic Receptor ◽  
Adrenergic Receptor ◽  
Smooth Muscles ◽  
Maximal Effect ◽  
Krebs Solution ◽  
Contractile Responses ◽  
Longitudinal Smooth Muscle ◽  
M3 Receptor

The aim of the study was to investigate Simo decoction–induced contractions of antral smooth muscles of rats and its mechanisms. The contractile responses of longitudinal strips to consecutive concentrations of Simo decoction were characterized by atropine, gallamine, 4-diphenylacetoxy-N-methylpiperidine methiodide, and adrenaline, hexamethonium, L-arginine, and nifedipine and compared with Krebs solution (control) and acetylcholine-induced contractions. Simo decoction dose-dependently increased contractions of antral strips ( P = .000 vs control); its maximal effect was higher than acetylcholine (10−3 mol L−1; P < .05); Simo decoction–induced contractions were completely inhibited by atropine, 4-diphenylacetoxy-N-methylpiperidine methiodide, or 4-diphenylacetoxy-N-methylpiperidine methiodide + gallamine ( P = .000 for all) but were partly suppressed by gallamine, adrenaline, hexamethonium, L-arginine, and nifedipine ( P = .000 for all). Simo decoction promotes the contractions of antral strips mainly through activation of muscarinic M3 receptor, while partly through activation of M2 receptor, Ca2+ channel, nicotinic receptor, and inhibition of adrenergic receptor as well as release of nitric oxide.

Regulation of intracellular Ca2+ release in corpus cavernosum smooth muscle: synergism between nitric oxide and cGMP

2005 ◽  
Vol 288 (3) ◽  
pp. C650-C658 ◽  
Author(s):  
Beatrice A. Williams ◽  
Caiqiong Liu ◽  
Ling DeYoung ◽  
Gerald B. Brock ◽  
Stephen M. Sims
Keyword(s):  
Nitric Oxide ◽  
Smooth Muscle ◽  
Cellular Response ◽  
Contractile Response ◽  
Corpus Cavernosum ◽  
Soluble Guanylyl Cyclase ◽  
Adrenergic Stimulation ◽  
No Donor ◽  
No Donors ◽  
Intracellular Ca

Tonic contraction of corpus cavernosum smooth muscle cells (SMCs) maintains the flaccid state of the penis, and relaxation is initiated by nitric oxide (NO), leading to erection. Our aim was to investigate the effect of NO on the smooth muscle cellular response to adrenergic stimulation in corpus cavernosum. Fura-2 fluorescence was used to record intracellular Ca2+ concentration ([Ca2+]i) from freshly isolated SMCs from rat and human. Phenylephrine (PE) transiently elevated [Ca2+]i in the presence and absence of extracellular Ca2+, indicating release from intracellular stores. Whereas the NO donor S-nitroso- N-acetylpenicillamine (SNAP) with sildenafil citrate (SIL) caused no change in basal [Ca2+]i, the PE-induced rise of [Ca2+]i was reversibly inhibited by 27 ± 7% ( n = 21, P < 0.005) in rat and by 55 ± 15% ( n = 9, P < 0.01) in human SMCs. SNAP and SIL also reduced the contractile response to PE. To investigate the mechanism, we applied mediators alone or in combination. The soluble guanylyl cyclase inhibitor ODQ reduced the effect of SNAP and SIL. SIL, cGMP analogs, and NO donors without SIL did not reduce the PE-induced rise of [Ca2+]i. However, the combination of 8-bromo-cGMP with SNAP reduced the Ca2+ peak by 42 ± 9% ( n = 22, P < 0.01). Our results demonstrate that NO and cGMP act synergistically to reduce Ca2+ release from intracellular stores. Reduction of intracellular Ca2+ release may contribute to relaxation of the corpus cavernosum, leading to erection.

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