Antihistamines and vascular reactivity

1965 ◽  
Vol 209 (3) ◽  
pp. 545-549 ◽  
Author(s):  
Burton M. Altura ◽  
Benjamin W. Zweifach

The purpose of the present set of experiments was to determine the contribution of the dilator principle, histamine, to peripheral vascular homeostasis. This was done by means of direct microscopic observation of the mesocecal microcirculation through the use of antihistamines. These drugs were found not only to produce a contraction of the microvessels but also to increase the responsiveness to topically applied cate-cholamines and antihistamines as well. The evidence does not preclude the possibility that histamine is a naturally occurring regulator of local tissue blood flow; but on the other hand, one cannot with any confidence accept this possibility.

2017 ◽  
Vol 102 (2) ◽  
pp. 228-244 ◽  
Author(s):  
Kameljit K. Kalsi ◽  
Scott T. Chiesa ◽  
Steven J. Trangmar ◽  
Leena Ali ◽  
Makrand D. Lotlikar ◽  
...  

2003 ◽  
Vol 94 (1) ◽  
pp. 60-68 ◽  
Author(s):  
Takashi Miyauchi ◽  
Seiji Maeda ◽  
Motoyuki Iemitsu ◽  
Tsutomu Kobayashi ◽  
Yoshito Kumagai ◽  
...  

Nitric oxide (NO) is produced in the vascular endothelium and is a potent vasodilator substance that participates in the regulation of local vascular tone. Exercise causes peculiar changes in systemic and regional blood flow, i.e., an increase of systemic blood flow and a redistribution of local tissue blood flow, by which the blood flow is greatly increased in the working muscles, whereas it is decreased in some organs such as the kidney and intestine. Thus we hypothesized that exercise causes a tissue-specific change of NO production in some internal organs. We studied whether exercise affects expression of NO synthase (NOS) mRNA and protein, NOS activity, and tissue level of nitrite/nitrate (stable end products of NO) in the kidneys (in which blood flow during exercise is decreased) and lungs (in which blood flow during exercise is increased with the increase of cardiac output) of rat. Rats ran on a treadmill for 45 min at a speed of 25 m/min. Immediately after this exercise, kidneys and lungs were quickly removed. Control rats remained at rest during this 45-min period. Expression of endothelial NOS (eNOS) mRNA in the kidneys was markedly lower in exercise rats than in control rats, whereas that in the lungs was significantly higher in exercise rats than in control rats. Western blot analysis confirmed down- and upregulation of eNOS protein in the kidney and lung, respectively, after exercise. On the other hand, neither expression of neuronal NOS (nNOS) mRNA and nNOS protein nor inducible NOS (iNOS) mRNA and iNOS protein in the kidneys and lungs differed between exercise and control rats. NOS activity in the kidney was significantly lower in exercise rats than in control rats, whereas that in the lung was significantly higher in exercise rats than in control rats. On the other hand, the iNOS activity in the kidneys and lungs did not differ between exercise rats and control rats. Tissue nitrite/nitrate level in the kidneys was markedly lower in exercise rats, whereas that in the lungs was significantly higher in exercise rats. The present results show that production of NO is markedly and tissue-specifically changed in the kidney and lung by exercise.


2016 ◽  
Vol 48 (2) ◽  
pp. 116-123 ◽  
Author(s):  
José R. Lemos ◽  
Cleber R. Alves ◽  
Sílvia B. C. de Souza ◽  
Julia D. C. Marsiglia ◽  
Michelle S. M. Silva ◽  
...  

Besides neuronal plasticity, the neurotrophin brain-derived neurotrophic factor (BDNF) is also important in vascular function. The BDNF has been associated with angiogenesis through its specific receptor tropomyosin-related kinase B (TrkB). Additionally, Val66Met polymorphism decreases activity-induced BDNF. Since BDNF and TrkB are expressed in vascular endothelial cells and aerobic exercise training can increase serum BDNF, this study aimed to test the hypotheses: 1) Serum BDNF levels modulate peripheral blood flow; 2) The Val66Met BDNF polymorphism impairs exercise training-induced vasodilation. We genotyped 304 healthy male volunteers (Val66Val, n = 221; Val66Met, n = 83) who underwent intense aerobic exercise training on a running track three times/wk for 4 mo. We evaluated pre- and post-exercise training serum BDNF and proBDNF concentration, heart rate (HR), mean blood pressure (MBP), forearm blood flow (FBF), and forearm vascular resistance (FVR). In the pre-exercise training, BDNF, proBDNF, BDNF/proBDNF ratio, FBF, and FVR were similar between genotypes. After exercise training, functional capacity (V̇o2 peak) increased and HR decreased similarly in both groups. Val66Val, but not Val66Met, increased BDNF (interaction, P = 0.04) and BDNF/proBDNF ratio (interaction, P < 0.001). Interestingly, FBF (interaction, P = 0.04) and the FVR (interaction, P = 0.01) responses during handgrip exercise (HG) improved in Val66Val compared with Val66Met, even with similar responses of HR and MBP. There were association between BDNF/proBDNF ratio and FBF (r = 0.64, P < 0.001) and FVR (r = −0.58, P < 0.001) during HG exercise. These results show that peripheral vascular reactivity and serum BDNF responses to exercise training are impaired by the BDNF Val66Met polymorphism and such responsiveness is associated with serum BDNF concentrations in healthy subjects.


1981 ◽  
Vol 241 (1) ◽  
pp. G1-G15 ◽  
Author(s):  
K. M. Walus ◽  
E. D. Jacobson

Effects of muscular activity on local blood flow have been delineated in other muscular organs but are part of a complex relationship in the small intestine. Some of our inability to provide a clear picture of the circulatory events surrounding intestinal motility relates to the variety of imprecise techniques that have been used to explore the relationship. Distension of the gut impedes blood flow through the intestinal wall, especially in the mucosa. Stimulation of motility evokes more variable responses in the intestinal circulation, including increases in blood flow; however, the circulatory response reflects mostly the nature of the intervention used to activate motility. Many motor stimuli in the gut have intrinsic vasoactive properties. Spontaneous motor events seem to have only small effects on total blood flow to the small intestine. Reduction in blood flow to the gut evokes initial increases in motility followed by inhibition of motor activity. Products of metabolism in the intestine influence both motor and vascular reactivity. More sensitive methods need to be developed to separate the types of intestinal motor activity, to localize mechanical events in specific sites in the wall of the gut, to better record electrical correlates of motility, and to measure local tissue blood flow. These technical developments will permit delineation of the linkage between motor and vascular events and should identify the regulatory factors.


2004 ◽  
Vol 106 (1) ◽  
pp. 19-25 ◽  
Author(s):  
N. ANIM-NYAME ◽  
S. R. SOORANNA ◽  
M. R. JOHNSON ◽  
M. H. SULLIVAN ◽  
J. GAMBLE ◽  
...  

There is evidence that tissue blood flow is regulated by retrograde transmission of signals initiated at capillary and post-capillary sites, and transmitted via the endothelium to modulate pre-capillary resistance. We have used pre-eclampsia as a model to test the hypothesis that normal endothelium is required to enable adjustment of blood flow to match tissue requirements. Integrity of the endothelial pathway was assessed by measuring calf blood flow at increasing venous pressures, using an established small cumulative-step venous-congestion plethysmography protocol in ten women with pre-eclampsia, 17 normal pregnant controls and ten non-pregnant women. Endothelial cell activation was assessed by measuring plasma levels of the cell adhesion molecules, intercellular cell-adhesion molecule-1 (ICAM-1), vascular cell-adhesion molecule-1 (VCAM-1) and E-selectin. Baseline calf blood flow was significantly lower in pre-eclampsia than in the other two groups (P<0.0001; ANOVA). In the pre-eclampsia group, there was a fall in blood flow as venous congestion pressure was raised (P<0.0001; ANOVA). No such change was observed in the other two groups. A significant inverse correlation was observed between the reduction in blood flow in pre-eclampsia and the levels of E-selectin (r=-0.92, P=0.0002), VCAM-1 (r=-0.93, P=0.0008) and ICAM-1 (r=-0.86, P=0.001). The differences between the pre-eclamptic women and the other two groups support the notion that the failure to sustain blood flow during a cumulative pressure step protocol in the pre-eclamptic group might be influenced by interference with the retrograde transmission of signals via the endothelium in these patients.


1991 ◽  
Vol 261 (6) ◽  
pp. R1579-R1586 ◽  
Author(s):  
A. M. Lacombe ◽  
D. R. Jones

Circulating catecholamines increase by three orders of magnitude in forced submerged ducks; their role in promoting vascular resistance was studied using vascular perfusion of hindlimbs. Perfusion pressure and blood flow were recorded simultaneously in hindlimbs of ducks during forced submergence. One leg was perfused with blood mixtures devoid of catecholamines (test leg) and compared with the other autoperfused leg. Perfusion pressures in test legs perfused with hyperoxic and hypocapnic blood or with hypoxic and hypocapnic blood were not significantly different from those in the matching autoperfused legs. However, when test legs were perfused with hypercapnic blood, regardless of whether blood was hypoxic or hyperoxic, perfusion pressures were significantly lower than in autoperfused legs. Adding catecholamines to test legs perfused with hypoxic and hypercapnic blood, after 3 min submergence, significantly enhanced vasoconstriction. Hypercapnia acts directly on the peripheral vascular beds and impairs the neurally mediated vasoconstriction during submergence, while circulating catecholamines restore peripheral vasoconstriction. Thus circulating catecholamines are needed to compensate for the depressant action of hypercapnia on neurally mediated vasoconstriction.


1972 ◽  
Vol 68 (2_Supplb) ◽  
pp. S95-S111 ◽  
Author(s):  
Niels A. Lassen ◽  
Ole Andrée Larsen

ABSTRACT Indicators which freely cross the capillary wall can be used for measurement of tissue blood flow in many different ways. Basically one can distinguish two categories of methods, viz. the ones where the indicator enters the tissue via the inflowing blood and the ones where the indicator is deposited locally in the tissue. The most important methods are briefly described with special emphasis on the theory of blood flow measurement.


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