Role of EDRF/NO in regional vascular resistance in pharmacologically denervated rats

1996 ◽  
Vol 3 (3) ◽  
pp. 149-156
Author(s):  
Taku Yamashita ◽  
Ichiro Kuwahira ◽  
Shigeru Harasawa ◽  
Takeshi Miwa ◽  
Tetsuo Oka ◽  
...  
Keyword(s):  
Vascular Resistance ◽  
Regional Vascular Resistance

Ghrelin and Obesity-An Update

2017 ◽  
Vol 9 (1) ◽  
Author(s):  
Gandhi M. ◽  
Swaminathan S.
Keyword(s):  
Diabetes Mellitus ◽  
Cardiac Output ◽  
Energy Balance ◽  
Vascular Resistance ◽  
The Body ◽  
Ghrelin Receptor ◽  
Type2 Diabetes ◽  
Type2 Diabetes Mellitus ◽  
Natural Hormones

Ghrelin as human natural hormones is involved in fundamental regulatory process of eating and energy balance. It is a stomach derived hormone that acts as at the ghrelin receptor in multiple tissues throughout to the body. Its properties includes increasing appetite, decreasing systemic inflammation, decreasing vascular resistance ,increasing cardiac output, increasing glucose and IGF-1 levels, Hence it may play a significant role in Diabetes mellitus. Many studies have linked ghrelin to obesity and this paper is an attempt to bring out recent findings on the role of ghrelin in Diabetes Mellitus, particularly type2 Diabetes mellitus.

scholarly journals Portal hypertensive response to kinin

2009 ◽  
Vol 81 (3) ◽  
pp. 431-442 ◽  
Author(s):  
Maria Kouyoumdjian ◽  
Marcia R. Nagaoka ◽  
Mauricio R. Loureiro-Silva ◽  
Durval R. Borges
Keyword(s):  
Vascular Resistance ◽  
Rat Liver ◽  
Liver Perfusion ◽  
Stellate Cells ◽  
Kinin System ◽  
Rat Liver Perfusion ◽  
Isolated Liver Cells ◽  
B2 Receptors ◽  
Intrahepatic Vascular Resistance

Portal hypertension is the most common complication of chronic liver diseases, such as cirrhosis. The increased intrahepatic vascular resistance seen in hepatic disease is due to changes in cellular architecture and active contraction of stellate cells. In this article, we review the historical aspects of the kallikrein-kinin system, the role of bradykinin in the development of disease, and our main findings regarding the role of this nonapeptide in normal and experimentalmodels of hepatic injury using the isolated rat liver perfusion model (mono and bivascular) and isolated liver cells. We demonstrated that: 1) the increase in intrahepatic vascular resistance induced by bradykinin is mediated by B2 receptors, involving sinusoidal endothelial and stellate cells, and is preserved in the presence of inflammation, fibrosis, and cirrhosis; 2) the hepatic arterial hypertensive response to bradykinin is calcium-independent and mediated by eicosanoids; 3) bradykinin does not have vasodilating effect on the pre-constricted perfused rat liver; and, 4) after exertion of its hypertensive effect, bradykinin is degraded by angiotensin converting enzyme. In conclusion, the hypertensive response to BK is mediated by the B2 receptor in normal and pathological situations. The B1 receptor is expressed more strongly in regenerating and cirrhotic livers, and its role is currently under investigation.

Reflex effects of thoracic aorta wall stretch on regional vascular resistance

1978 ◽  
Vol 56 (3) ◽  
pp. 390-394
Author(s):  
Peter M. Szeto ◽  
Franco Lioy
Keyword(s):  
Arterial Pressure ◽  
Thoracic Aorta ◽  
Vascular Resistance ◽  
Carotid Arteries ◽  
Peripheral Resistance ◽  
Adrenergic Blockade ◽  
Vascular Responses ◽  
Regional Vascular Resistance ◽  
Vascular Beds ◽  
Intact Limb

In anesthetized, vagotomized cats with both carotid arteries occluded, a stretch of the walls of the thoracic aorta, performed without obstructing aortic flow, induced a significant reflex increase in arterial pressure (35 ± 2−26 ± 1 mmHg; systolic–diastolic). This pressure increase was accompanied by significant increases in peripheral resistance in the superior mesenteric (+30%), renal (+23%), and external iliac (+23%) vascular beds. The increase in iliac resistance observed in the skinned leg was comparable with that observed in the contralateral intact limb. All these vascular responses were drastically reduced by the administration of phenoxybenzamine. After α-adrenergic blockade no signs of reflex vasodilatation could be detected during aortic stretch in any of the vascular beds examined.

scholarly journals Role of Renocortical Cyclooxygenase-2 for Renal Vascular Resistance and Macula Densa Control of Renin Secretion

2001 ◽  
Vol 12 (5) ◽  
pp. 867-874
Author(s):  
HAYO CASTROP ◽  
FRANK SCHWEDA ◽  
KARL SCHUMACHER ◽  
KONRAD WOLF ◽  
ARMIN KURTZ
Keyword(s):  
Vascular Resistance ◽  
Macula Densa ◽  
Renal Vascular Resistance ◽  
Renin Secretion ◽  
Expression Level ◽  
Flow Rates ◽  
Low Salt ◽  
Cox 2 ◽  
Renal Vascular

Abstract. This study aimed to assess the role of cyclooxygenase-2 (COX-2)-derived prostanoids for the macula densa control of renal afferent arteriolar resistance and for renin secretion. For this purpose, studied were the effects of blocking macula densa salt transport by the loop diuretic bumetanide (100 μM) on renal perfusate flow and on renin secretion in isolated perfused rats, in which renocortical COX-2 expression was prestimulated in vivo by treatment with the angiotensin-converting enzyme inhibitor ramipril, with low-salt diet, or with a combination of both. These maneuvers stimulated COX-2 expression in an order of ramipril + low salt ≫ low salt > ramipril > controls. Flow rates through isolated kidneys at a constant pressure of 100 mmHg were dependent on the pretreatment regimen, in the way that they went in parallel with COX-2 expression. The COX-2 inhibitor NS-398 (10 μM) lowered flow rates depending on the COX-2 expression level and was most pronounced therefore after pretreatment with low salt + ramipril. NS-398 did not change the increase of flow in response to bumetanide but attenuated the stimulation of renin secretion in response to bumetanide in a manner depending on the expression level of COX-2. These findings suggest that in states of increased renocortical expression of COX-2, overall renal vascular resistance and the macula densa control of renin secretion become dependent on COX-2—derived prostanoids.

scholarly journals ROLE OF HYPOKALEMIA IN VASCULAR RESISTANCE TO ANGIOTENSIN II (AII)

1977 ◽  
Vol 11 (4) ◽  
pp. 430-430
Author(s):  
N Radfar ◽  
J R Gill ◽  
A A Taylor ◽  
F C Bartter
Keyword(s):  
Angiotensin Ii ◽  
Vascular Resistance

PERIPHERAL CIRCULATORY RESPONSE TO FEEDING IN THE NEWBORN INFANT

PEDIATRICS ◽  
1971 ◽  
Vol 47 (2) ◽  
pp. 378-383
Author(s):  
Alice C. Yao ◽  
C. Göran Wallgren ◽  
Sachchida N. Sinha ◽  
John Lind
Keyword(s):  
Vascular Resistance ◽  
Venous Occlusion ◽  
Term Infants ◽  
Significant Drop ◽  
Circulatory Response ◽  
Control Value ◽  
Limb Perfusion ◽  
Normal Term ◽  
Regional Vascular Resistance ◽  
Umbilical Arterial Catheter

The peripheral circulatory response to feeding was studied in 39 normal term infants, age ranging from 24 hours to 9 days. Blood flow to calf of left leg was measured by the venous occlusion plethysmographic method before and half hourly after feeding for 3 to 3½ hours. Arterial pressure was monitored in nine infants via an umbilical arterial catheter simultaneously and regional vascular resistance to flow in the leg calculated. Changes in pulse rate, and skin and rectal temperatures were also monitored. A significant drop in the calf perfusion averaging 49% of the control value was observed at the 30 minutes postprandial recording. This was due to an increased regional vascular resistance and blood pressure remained unchanged during the time of study. As a rule, a superseding hyperperfusion of the limb overshooting the control value by 40 to 50% occurred 1½ to 3 hours after feeding. This was comparable to the hyperkinetic phase described in adult man and other species after meals. The early postprandial vasoconstriction in the leg seems unique to the newborn. It is suggested that having the early circulatory demand provoked by feeding is relatively bigger in the newborn than in the adult and is met partly at the expense of lower limb perfusion.

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