Morphological and functional alterations of mesenteric small resistance arteries in early renal hypertension in rats

1991 ◽  
Vol 261 (4) ◽  
pp. H1171-H1177 ◽  
Author(s):  
L. Y. Deng ◽  
E. L. Schiffrin
Keyword(s):  
Blood Vessels ◽  
Vascular Reactivity ◽  
Rapid Development ◽  
Renal Hypertension ◽  
Lumen Diameter ◽  
External Diameter ◽  
Effective Pressure ◽  
Resistance Arteries ◽  
Hypertensive Rats ◽  
Small Resistance

We investigated the structure and reactivity of small resistance arteries of two-kidney, one-clip (2K,1C) and one-kidney, one-clip (1K,1C) Goldblatt hypertensive rats within 4-6 wk of development of hypertension. Blood vessels from the mesenteric vascular bed with lumen diameter less than 300 microns were mounted on a wire myograph. The media of the vessel wall was significantly increased and lumen diameter was decreased in 2K,1C and 1K,1C rats. External diameter of blood vessels was reduced in both 2K,1C and 1K,1C rats, whereas cross-sectional area of the wall was increased significantly in 1K,1C rats. Wall tension in response to KCl was significantly lower in 2K,1C and 1K,1C hypertensive rats, whereas tension in response to norepinephrine (NE) was reduced in 1K,1C hypertensive rats but was similar in 2K,1C rats and controls. Active tension in response to arginine vasopressin (AVP) was similar in all groups. As a consequence of the reduced lumen circumference of small arteries, effective pressure in response to NE was similar in hypertensive and control rats, whereas effective pressure in response to AVP was exaggerated in the hypertensive rats. The sensitivity to NE and AVP was similar in all groups. These results show the rapid development of functional and structural changes in small resistance arteries in renal hypertensive rats within 4-6 wk of hypertension, with significant reduction in external and lumen diameters, increased media width, and increased media-to-lumen ratio, which enhance vascular reactivity to vasoconstrictors, in particular NE and AVP.

ABSORPTION SPECTROSCOPY FOR THE ASSESSMENT OF SMALL-ARTERY STRUCTURE

2001 ◽  
Vol 13 (04) ◽  
pp. 175-180
Author(s):  
A. KAUR ◽  
H. FISH ◽  
H. THURSTON ◽  
P. R. SMITH
Keyword(s):  
Blood Vessels ◽  
Transmission Spectra ◽  
Resistance Arteries ◽  
Hypertensive Rats ◽  
Arterial Blood ◽  
Spectroscopic Examination ◽  
Normal Rat ◽  
Small Resistance ◽  
Quasi Newton ◽  
First Time

The assessment of vascular structure gives important information on pathological processes, particularly for the investigation of diseased vessels. In this study the Mulvany wire myogarph is adapted for spectroscopic examination of small arterial blood vessels obtained from hypertensive and normal rat specimens. An experimental study of 20 vessels obtained from adult Wistar rats and Goldblatt (one kidney one clip) hypertensive rats was carried out. Segments of small resistance arteries mounted under isometric conditions on a wire myograph and set to normalised conditions of passive force directly obtained from its circumferential length-tension relationship were morphologically examined and transmission spectra obtained. Features of the observed transmission spectra were extracted by means of an empirical non-linear model using the quasi-Newton method. These features were correlated for the first time with standard descriptors of vessel morplzology, media:lumen ratio and with arterial blood pressure. The extent and significance of such correlations are sufficient to distinguish the presence of hypertension in isolated arterial segments from hypertensive animals. This technique may provide an alternative to light microscopy as well as a potential new tool for the analysis of small blood vessels in the study of vascular disease.

Effects of endothelin on resistance arteries of DOCA-salt hypertensive rats

1992 ◽  
Vol 262 (6) ◽  
pp. H1782-H1787 ◽  
Author(s):  
L. Y. Deng ◽  
E. L. Schiffrin
Keyword(s):  
Lumen Diameter ◽  
Acute Effects ◽  
Resistance Arteries ◽  
Hypertensive Rats ◽  
Cross Sectional ◽  
Functional Changes ◽  
Tension Response ◽  
Maximal Tension ◽  
Nonionic Detergent ◽  
Small Resistance

The effect of endothelin (ET)-1 was investigated on resistance arteries of less than 300-microns lumen diameter from the mesenteric circulation, mounted on a wire myograph, in deoxycorticosterone acetate (DOCA)-salt hypertensive rats within 2 wk of developing hypertension and in uninephrectomized controls. Arteries from DOCA-salt hypertensive rats presented a significantly reduced external and lumen diameter and increased media width and wall cross-sectional area. Vessels from DOCA-salt hypertensive rats responded to ET-1 with lower active wall tension and media stress. Because the lumen diameter was significantly decreased in DOCA-salt hypertensive rats, the active pressure developed in response to ET-1 was similar in both groups. In contrast, the maximal tension response to arginine vasopressin was enhanced in DOCA-salt hypertensive rats. The sensitivity to both peptides and norepinephrine (NE) was similar in both groups. After removal of endothelium by exposure to the nonionic detergent 3-[(3-cholamidopropyl)dimethylammonio]-1-propanesulfonate, ET-1 elicited tension responses that were also lower in DOCA-salt hypertensive rats, whereas NE responses were similar in both groups. These results demonstrate significant morphological and functional changes in small arteries of DOCA-salt hypertensive rats within 2 wk of developing hypertension and blunted reactivity to ET-1. Because similar results were found after removal of endothelium, it is likely that neither prior receptor occupation by endogenous ET nor acute effects of other endothelial cell products play a role in the reduced responsiveness to ET of vascular smooth muscle of small resistance arteries of DOCA-salt hypertensive rats.

Intracellular signal transduction for vasoactive peptides in hypertension

1994 ◽  
Vol 72 (8) ◽  
pp. 954-962 ◽  
Author(s):  
Ernesto L. Schiffrin
Keyword(s):  
Signal Transduction ◽  
Smooth Muscle ◽  
Angiotensin Ii ◽  
Blood Vessels ◽  
Vascular Reactivity ◽  
Inositol Phosphate ◽  
Cytosolic Calcium ◽  
Resistance Arteries ◽  
Intracellular Signal Transduction ◽  
Intracellular Signal

Increased peripheral resistance is the hallmark of hypertension. It may result in part from exaggerated vascular reactivity of resistance arteries. Some changes in density of surface receptors for different vasoconstrictors and vasorelaxants have been described that could play a role in physiological findings in hypertension. Smooth muscle cells of resistance arteries have increased cytosolic free calcium concentration in some models of experimental hypertension, which may contribute to enhance vascular responses. Exaggerated response of the inositol phosphate – calcium pathway has been demonstrated after stimulation with some vasoconstrictor agents such as norepinephrine, angiotensin II, and vasopressin. In contrast, responses to the potent vasoconstrictor peptide endothelin-1 are either normal (in spontaneously hypertensive rats) or blunted (in deoxycorticosterone-salt hypertension). In the latter case, endothelin receptor density, inositol phosphate and diacylglycerol generation, and cytosolic calcium responses agree with blunted response of blood vessels. Increased basal cytosolic calcium and exaggerated sensitivity of myosin light chain to calcium may be mechanisms underlying increases in sensitivity of signal transduction in smooth muscle in some models of hypertension. However, in general, signal transduction of receptors for vasoconstrictors appears to be blunted rather than exaggerated, except for responses to angiotensin II. Altered structure of resistance arteries (remodeling) may be a mechanism that, even in presence of blunted intracellular signal transduction, may result in enhanced pressor responsiveness of blood vessels in hypertension.Key words: second messengers, phospholipases, inositol phosphates, calcium, magnesium, Na+–H+ exchange, protein kinases, cyclic nucleotides, vascular reactivity.

Abstract P267: Arbidol, A Targeted Covid-19 Therapy, Inhibited Contractile Responses To Phenylephrine In Mesenteric Arteries And Aortas Of Hypertensive Rats

Hypertension ◽  
2021 ◽  
Vol 78 (Suppl_1) ◽  
Author(s):  
Olufunke O Arishe ◽  
Stephanie Wilczynski ◽  
Anna Thamasett ◽  
Clinton R Webb
Keyword(s):  
Lipid Membranes ◽  
Vascular Reactivity ◽  
Viral Infections ◽  
Mesenteric Arteries ◽  
Resistance Arteries ◽  
Adrenergic Stimulation ◽  
Hypertensive Rats ◽  
Contractile Responses ◽  
Viral Attachment

Background: Hypertension is the most prevalent comorbidity of COVID-19 infection. This infection is caused by the severe acute respiratory syndrome coronavirus SARS-CoV-2. SARS-CoV-2 is a single-stranded RNA and could activate the endosomal Toll-like receptor 7 (TLR7), indicating a vital role of the receptor in its therapeutic target. Studies have reported that the lysosomotropic drug chloroquine has antihypertensive effects through its action on inhibiting the endosomal TLRs. Arbidol is a potential broad-spectrum antiviral used in the treatment of many viral infections including influenza. Arbidol prevents viral infection by interacting with aromatic acids; arbidol also binds to lipid membranes, altering the configuration of the cytoplasm or endosome. Wang et al., in 2020 reported that arbidol effectively inhibited the coronavirus SARS-CoV-2 in vitro by impeding viral attachment and release from the endolysosomes. Hypothesis: We hypothesized that arbidol would improve vascular reactivity in hypertension. Methods: We studied the effects of arbidol on the contractility of mesenteric resistance arteries (MRA) and aortas of male Wistar rats (20 weeks old, n=4) and spontaneously hypertensive rats (SHR) (20 weeks old, n=4) on a myograph by incubating the arterial rings with 10μM arbidol (Sigma, USA.) or vehicle (DMSO) for 30 mins. Statistical analysis was performed using nonlinear regression, and one- and two-way ANOVAs. Results: Arbidol (10 μM) impaired the contractile responses of MRA and aorta from normotensive and hypertensive rats to phenylephrine (PE). MRA Wistar: (pEC50 6.11 ± 0.15 vs 3.42 ± 0.38), SHR: (5.89 ± 0.19 vs 3.56 ± 0.19) and aorta Wistar: (pEC 50 7.49 ± 0.19 vs 5.97 ± 0.14), SHR (pEC50 7.14 ± 0.31 vs 4.41 ± 0.15). The arbidol-induced impaired contraction to PE was greater in the SHR aorta compared with the Wistar aorta. After washing out the drug, the arterial rings contracted to 120mM KCl at the same magnitude as the initial contraction to 120mM KCl. Conclusions: Our data demonstrate that arbidol impairs vascular contractile responses to α-adrenergic stimulation, with a greater response in the hypertensive rats. This indicates antihypertensive effects potentially through the regulation of TLR signaling.

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