α1D-Adrenergic Receptor Knockout Mice Display Impaired Vascular Contractile Response to Catecholamines

Author(s):  
Gozoh Tsujimoto ◽  
Akito Tanoue
2013 ◽  
Vol 35 (3) ◽  
Author(s):  
Anderson Carlos Marçal ◽  
Ana Paula Couto Davel ◽  
Angelo Rafael Carpinelli ◽  
Patrícia Chakur Brum ◽  
Luciana Venturini Rossoni ◽  
...  

2011 ◽  
Vol 25 (S1) ◽  
Author(s):  
Ashley Nicole Guillory ◽  
Cori S. Wijaya ◽  
Abeer Rababa'h ◽  
Xing Yin ◽  
Bradley K. McConnell

1982 ◽  
Vol 243 (5) ◽  
pp. H748-H753 ◽  
Author(s):  
J. C. Longhurst ◽  
J. Ibarra

There is presently little information on the efferent mechanisms responsible for the reflex cardiovascular activation during passive gastric distension. Therefore, 40 cats anesthetized with alpha-chloralose were studied with passive gastric balloon distention before and during 1) two repeated gastric distensions, 2) beta-adrenergic blockade with propranolol, 3) alpha-adrenergic blockade with phentolamine, or 4) bilateral adrenalectomy. Before and during each distension mean arterial pressure, heart rate, cardiac output, rate of rise of left ventricular pressure (dP/dt) at 40 mmHg developed pressure and calculated systemic vascular resistance were determined. Repeated gastric distension caused similar hemodynamic responses without tachyphylaxis. beta-Blockade significantly reduced the increase in dP/dt from 893 +/- 362 to 150 +/- 63 mmHg/s. alpha-Blockade significantly altered the changes in mean arterial pressure from 33 +/- 5.0 to -2 +/- 4.7 mmHg and systemic vascular resistance from 0.114 +/- 0.019 to 0.004 +/- 0.031 peripheral resistance units. Bilateral adrenalectomy significantly diminished the contractile response from 525 +/- 107 to 50 +/- 85 mmHg/s but did not significantly alter the pressor and vasoconstrictor responses. We conclude that, during passive gastric distension in cats, the increase in myocardial contractility is mediated by beta-adrenergic-receptor stimulation, whereas the arterial vasoconstrictor and pressor responses are mediated by alpha-adrenergic receptor stimulation. Additionally, during gastric distension a substantial portion of the contractile response is dependent on the integrity of the adrenal glands.


2006 ◽  
Vol 0 (0) ◽  
pp. 070209222715079-???
Author(s):  
Daniel Chesik ◽  
Lisa Glazenburg ◽  
Jacques De Keyser ◽  
Nadine Wilczak

Neuroscience ◽  
2002 ◽  
Vol 113 (2) ◽  
pp. 289-299 ◽  
Author(s):  
J Lähdesmäki ◽  
J Sallinen ◽  
E MacDonald ◽  
B.K Kobilka ◽  
V Fagerholm ◽  
...  

1999 ◽  
Vol 56 (1) ◽  
pp. 154-161 ◽  
Author(s):  
John D. Altman ◽  
Anne U. Trendelenburg ◽  
Leigh MacMillan ◽  
Dan Bernstein ◽  
Lee Limbird ◽  
...  

2019 ◽  
Author(s):  
Kawin Padmaja Marconi ◽  
Bhavithra Megan ◽  
Alen Major Venis ◽  
Renu Raj ◽  
Sathya Subramani

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.


1996 ◽  
Vol 270 (3) ◽  
pp. H915-H923 ◽  
Author(s):  
L. D. Longo ◽  
N. Ueno ◽  
Y. Zhao ◽  
L. Zhang ◽  
W. J. Pearce

Adrenergic-mediated responses in cerebral vessels in vitro differ with vessel segment. We performed this study to test the hypothesis that these vessel-specific cerebral artery norepinephrine (NE)-induced contractility changes are mediated in part by differences in alpha 1-adrenergic receptor (alpha 1-R) density (Bmax) or antagonist dissociation constant (KD), and/or inositol 1,4,5-trisphosphate [Ins(1,4,5)P3] synthesis. In common carotid (Com), circle of Willis (Wil), and middle cerebral arteries (MCA) from adult sheep we measured NE-induced contractions. We also quantified alpha 1-R in these, and in anterior, middle, and posterior (AMP) cerebral arteries and cerebral microvessels (Micro). In addition, we quantified NE-induced Ins(1,4,5)P3 synthesis. pD2 values of Com and MCA were 5.2 +/- 0.1 and 6.3 +/- 0.1, respectively. In contrast, the MCA maximum response to NE compared with K+ was much lower than that of the Com. In the Com, Wil, AMP, and Micro, alpha 1-R Bmax was 54 +/- 3, < 5 +/- 2, 23 +/- 3, and 35 +/- 3 fmol/mg protein, respectively. KD averaged 0.20 +/- 0.05 nM in the several vessel groups. In Com and in AMP cerebral arteries, NE produced a rapid increase in Ins(1,4,5)P3 with a peak at 45 s, and 50% effective concentration of 5.5 +/- 0.2 microM. NE stimulated a 240% increase of Ins(1,4,5)P3 in both Com and AMP, whereas Wil showed essentially no response. The ovine MCA was more sensitive to NE than was the Com. In contrast, MCA showed a much lower maximum contractile response to NE compared with K+. Cerebral arteries (AMP) had only about half the alpha 1-R density of the Com. In AMP cerebral arteries, both the basal and NE-stimulated Ins(1,4,5)P3 values were much less than those of the Com. In MCA, the ratio of Ins(1,4,5)P3 response to alpha 1-R Bmax was much greater than in Com. These findings suggest important artery-to-artery differences in components of the cerebrovascular alpha 1-R-mediated contractile pathway. They also suggest considerable potential for modulation of pharmacomechanical coupling and homeostatic regulation of cerebrovascular tone.


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