scholarly journals Effects of Mandibular Extension on Pial Arteriolar Diameter Changes in Glucocorticoid-Induced Hypertensive Rats

2019 ◽  
Vol 10 ◽  
Author(s):  
Dominga Lapi ◽  
Maurizio Varanini ◽  
Lucrezia Galasso ◽  
Martina Di Maro ◽  
Giuseppe Federighi ◽  
...  
Keyword(s):  
Hypertensive Rats ◽  
Arteriolar Diameter

Afferent arteriolar diameter in DOCA-salt and two-kidney one-clip hypertensive rats

1983 ◽  
Vol 245 (6) ◽  
pp. F755-F762 ◽  
Author(s):  
B. M. Iversen ◽  
L. Morkrid ◽  
J. Ofstad
Keyword(s):  
Blood Pressure ◽  
Plasma Renin ◽  
Afferent Arteriole ◽  
Cortical Layers ◽  
Hypertensive Rats ◽  
Salt Hypertension ◽  
Nephron Loss ◽  
Microsphere Method ◽  
Arteriolar Diameter ◽  
Equal Thickness

The afferent arteriolar diameter (dAA) was investigated during development of hypertensive renal disease in normal and uninephrectomized control rats, in chronic DOCA-salt (DOCA), post-DOCA (p-DOCA), and chronic two-kidney one-clip (2K-1C) hypertensive rats, and in post-two-kidney one-clip (p-2K-1C) normotensive rats. dAA was measured by the microsphere method. Nephron loss was present in the kidneys exposed to elevate blood pressure. The dAA was reduced from 19.9 to 17.2 micron in the DOCA group (P less than 0.001) and from 19.1 to 16.3 micron in the nonclipped kidneys in the 2K-1C group (P less than 0.001). The dAA increased from 19.9 to 20.7 micron in the p-DOCA group. Afferent arteriolar dilatation from 19.1 to 21.0 micron (P less than 0.001) was present about 50 days after clipping in the 2K-1C group; in the clipped kidneys the dAA returned to normal (18.9 micron) after declipping. No relation between the dAA and plasma renin concentration was observed. In all models dAA was the same in three cortical layers of equal thickness. Accordingly, chronic renal DOCA-salt hypertension constricts the afferent arteriole with angiotensin-independent mechanisms. Autoregulatory dilatation of the afferent arteriole seems to be maintained for at least 50 days. When the hypertension is moderate, dAA in damaged kidneys may be dilated.

Endogenous vasoconstrictor tone in intestine of normal and portal hypertensive rats

1993 ◽  
Vol 264 (1) ◽  
pp. H171-H177 ◽  
Author(s):  
T. Joh ◽  
D. N. Granger ◽  
J. N. Benoit
Keyword(s):  
Blood Flow ◽  
Portal Hypertension ◽  
Adrenergic Receptors ◽  
Adrenergic Blockade ◽  
Ang Ii ◽  
Hypertensive Rats ◽  
Alpha Adrenergic Receptors ◽  
Control Plasma ◽  
Arteriolar Diameter

The purpose of the present study was to determine the effects of endogenous norepinephrine, vasopressin (AVP), and angiotensin II (ANG II) on normal intestinal microvascular dimensions and to determine whether endogenous vasoconstrictor tone was altered in chronic portal hypertension. The intestine of normal and portal hypertensive rats was prepared for in vivo microscopic observation, and an arteriole (1A, 2A, or 3A) was selected for study. Arteriolar diameter and erythrocyte velocity were continuously monitored and used in the calculation of arteriolar blood flow. Once steady-state conditions were established, specific antagonists to alpha-adrenergic, AVP, or ANG II receptors were applied locally to remove the influences of each of these systems. In normal animals, blockade of alpha-adrenergic receptors produced a 1.3, 1.5, and 14.7% increase in the diameter of 1A, 2A, and 3A, respectively. AVP blockade in normal animals produced an 8.7, 1.6, and 1.5% increase in the diameter of 1A, 2A, and 3A, respectively; ANG II blockade only produced an increase in 3A diameter (5.8%). alpha-Adrenergic blockade produced a smaller increase in portal hypertensive 3A diameter (2.3%) compared with normal rats. AVP and ANG II blockade produced a significantly larger dilation of 3A (AVP, 4.8%) and 1A (ANG II, 3.8%), respectively, compared with control. Plasma AVP and ANG II levels were higher in portal hypertensive (AVP, 9.1 pg/ml; ANG II, 8.6 pg/ml) than in normal rats (AVP, 5.5 pg/ml; ANG II, 6.6 pg/ml).(ABSTRACT TRUNCATED AT 250 WORDS)

Altered vascular norepinephrine responses in portal hypertensive intestine: role of PKA and guanylate cyclase

1997 ◽  
Vol 272 (4) ◽  
pp. G831-G837 ◽  
Author(s):  
Z. Y. Wu ◽  
J. N. Benoit
Keyword(s):  
Blood Flow ◽  
Protein Kinase ◽  
Guanylate Cyclase ◽  
Sprague Dawley ◽  
Hypertensive Rats ◽  
Cyclic Monophosphate ◽  
Selective Blockade ◽  
Before And After ◽  
Ly 83583 ◽  
Arteriolar Diameter

The purpose of the present study was to determine whether selective blockade of adenosine 3',5'-cyclic monophosphate (cAMP)- or guanosine 3',5'-cyclic monophosphate (cGMP)-mediated events modulated norepinephrine responses in intestinal microvessels of normal and portal hypertensive rats. Vascular norepinephrine responses were evaluated before and after inhibition of cAMP-dependent protein kinase [protein kinase A(PKA)] with Rp-adenosine 3',5'-cyclic monophosphothioate (Rp-cAMPS) or guanylate cyclase with LY-83583. Male Sprague-Dawley rats were divided into two groups: those with portal hypertension by portal vein stenosis and normal controls. The small intestine was prepared for microcirculatory studies. Arteriolar diameter and erythrocyte velocity were monitored, and microvascular flow was calculated from velocity and diameter data. The preparation was challenged with incremental concentrations of norepinephrine before and after addition of Rp-cAMPS (50 microM) or LY-83583 (30 microM). Arteriolar diameter and blood flow were significantly elevated in portal hypertensive rats; norepinephrine responses were significantly depressed. LY-83583 did not alter arteriolar diameter, blood flow, or norepinephrine responsiveness in normal or portal hypertensive rats. Rp-cAMPS did not affect arteriolar diameter, blood flow, or norepinephrine responsiveness in normal rats. However, in portal hypertensive rats, Rp-cAMPS reduced blood flow by approximately 20% (P < 0.05) and completely restored vascular norepinephrine responses to normal. The results indicate that cAMP- but not cGMP-dependent events are primarily responsible for the loss of microvascular norepinephrine responsiveness in portal hypertensive intestine.

scholarly journals Role of Purinoceptors in Regulating Afferent Arteriolar Diameter in DOCA‐salt Hypertensive Rats

2012 ◽  
Vol 26 (S1) ◽  
Author(s):  
Zhengrong Guan ◽  
Sean T Singletary ◽  
Anthony K Cook ◽  
Edward W Inscho
Keyword(s):  
Hypertensive Rats ◽  
Arteriolar Diameter

Potentiation of Bradykinin by Angiotensin-(1-7) on Resistance Vessels of Hypertensive Rats, Studied in Vivo .

Hypertension ◽  
2000 ◽  
Vol 36 (suppl_1) ◽  
pp. 696-696
Author(s):  
Liliam Fernandes ◽  
Zuleica B Fortes ◽  
Dorothy Nigro ◽  
Regina Scivoletto ◽  
Robson A S Santos ◽  
...  
Keyword(s):  
Topical Application ◽  
Ace Inhibition ◽  
Pharmacological Effects ◽  
Hypertensive Rats ◽  
Specific Receptor ◽  
Resistance Vessels ◽  
Before And After ◽  
Arteriolar Diameter

P19 Objective: To verify the Angiotensin-(1-7) [Ang-(1-7)]-activity on Bradykinin (BK)-induced vasodilation in SHR mesenteric arterioles, in vivo-in situ. Methods: Arteriolar diameter was measured by intravital microscopy before and after topical application of BK(1pmol), Acetylcholine(ACh 1.6nmol), Sodium nitroprusside (SNP 38pmol) or Histamine (5.4nmol) in the absence or presence of Ang-(1-7) (100pmol). To investigate the Ang-(1-7)/BK interaction, treatments were employed through topical application of antagonists of BK (HOE140,100pmol), Ang-(1-7)(A779,100pmol)and potassium channel (tetraethylammoniun - TEA,90pmol), with an inhibitor of NOSynthase (L-NAME 10nmol) and after cyclooxygenase blockade (indomethacin 5mg/Kg or diclofenac 2.5mg/Kg). To evaluate the effect of ACE- and/or AT 1 blockade on Ang-(1-7)/BK interaction, rats were treated for 21 days with enalapril, quinapril (10mg/Kg), losartan (15mg/Kg) or enalapril + losartan (10 and 15 mg/Kg, respectively). In those enalapril-treated rats the effect of BK (1pmol) was also analysed in the presence of A779 (100pmol). Results: BK-induced vasodilation, but not ACh, SNP or Histamine responses, was increased in the presence of Ang-(1-7) (4.96±0.7% vs 9.07±1.0% * ).This interaction was abolished by HOE (1.11±0.8% * ), A779 (5.13±0.6% * ), TEA (3.37±0.5% * ), indomethacin (1.73±0.4% * )and diclofenac (3.63±0.5% * ), whereas L-NAME did not modify the Ang-(1-7)-potentiating activity. The BK-potentiation by Ang-(1-7) was also observed after enalapril (10.57±0.5% * ), quinapril (8.9±0.7% * ), losartan (9.93±1.2% * ) and enalapril + losartan (10.59±0.5% * ). Enalapril increased the BK-vasodilation(8.21±0.7% * ), but this effect was reversed in the presence of A779 (4.27±0.5% * ). * p≤0.05 Conclusion: In the SHR microcirculation Ang-(1-7) potentiates BK through a specific receptor, probably releasing prostaglandins and EDHF. Our results indicate that the BK-potentiation by Ang-(1-7) may occur endogenously and contribute to the pharmacological effects of ACE inhibition. HOE 140 and Quinapril were gifts from HOECHST and Warner Lambert, respectively.

Segmental renal vascular resistance in the spontaneously hypertensive rat

1982 ◽  
Vol 242 (6) ◽  
pp. H961-H966 ◽  
Author(s):  
C. H. Hsu ◽  
J. H. Slavicek ◽  
T. W. Kurtz
Keyword(s):  
Vascular Resistance ◽  
Spontaneously Hypertensive Rat ◽  
Renal Vascular Resistance ◽  
Hypertensive Rats ◽  
Mean Values ◽  
Spontaneously Hypertensive ◽  
Microsphere Method ◽  
Wistar Kyoto ◽  
Renal Vascular ◽  
Arteriolar Diameter

Renal hemodynamics were studied during different stages of development of hypertension in unanesthetized spontaneously hypertensive rats (SHR). In SHR at 4 wks of age mean arterial pressure (MAP) was higher than in age-matched Wistar Kyoto rats (WKY); however, renal blood flow (RBF) and renal vascular resistance (RVR) were not different between these two groups. Mean values of RVR and MAP in 8- and 12-wk-old SHR were significantly greater than those of age-matched WKY. Both RBF of 8- and 12-wk-old SHR were significantly lower than the corresponding values of WKY. Afferent arteriolar diameter (AAD) was measured with a microsphere method. AAD was not different between 4-wk-old SHR and WKY; however, the AAD of 8-wk-old (16.3 +/- 0.23 micrometers, n = 5) and 12-wk-old (17.4 +/- 0.48, n = 5) SHR were significantly smaller than those of respective control WKY (17.3 +/- 0.34, n = 4, P less than 0.05; 19.3 +/- 0.12, n = 5, P less than 0.01). Calculated preglomerular (Rpre) and postglomerular resistances (Rpost) of 12-wk-old SHR were increased 96 and 129% when compared with respective segmental resistances of the control WKY. The decrease in AAD of 12-wk-old SHR was sufficient to account for a 33% increase in Rpre. After the rats were treated with hydralazine (0.5 mg/kg iv), MAP, RBF, and RVR of SHR were not different from the control WKY values. Rpre and Rpost of SHR were substantially decreased; however, vasodilation occurred at vessels proximal and distal to the afferent arteriole because AAD was not altered. Our results indicate that increased RVR in SHR involves increases in Rpre and Rpost.

Impairment of endothelium-dependent responses of cerebral arterioles in chronic hypertension

1987 ◽  
Vol 253 (6) ◽  
pp. H1435-H1440 ◽  
Author(s):  
W. G. Mayhan ◽  
F. M. Faraci ◽  
D. D. Heistad
Keyword(s):  
Cerebral Ischemia ◽  
Spontaneously Hypertensive Rats ◽  
Chronic Hypertension ◽  
Cerebral Microcirculation ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Vasoactive Substances ◽  
Cerebral Arterioles ◽  
Cerebral Vasodilator ◽  
Arteriolar Diameter

The goal of this study was to determine whether endothelium-dependent responses are impaired in the cerebral microcirculation of stroke-prone spontaneously hypertensive rats (SHRSP). We measured diameters of cerebral arterioles using intravital microscopy in normotensive rats (WKY) and SHRSP (6-8 mo old). Cerebral vasodilator responses to superfusion with adenosine, which is an endothelium-independent agonist, were similar in WKY and SHRSP. In contrast, cerebral vasodilator responses to superfusion with endothelium-dependent agonists were profoundly impaired in SHRSP. Acetylcholine (10(-4) M) increased pial arteriolar diameter 23 +/- 2% (means +/- SE) in WKY and did not change arteriolar diameter in SHRSP (-2 +/- 3%, P less than 0.05 vs. WKY). Serotonin (10(-5) M) increased pial arteriolar diameter 23 +/- 1% in WKY and, in contrast, reduced diameter 11 +/- 1% in SHRSP (P less than 0.05 vs. WKY). Nitroglycerin and acetylcholine produce vasodilatation by activation of guanosine 3',5'-cyclic monophosphate (cGMP). Nitroglycerin was used to determine whether impaired responses of cerebral arterioles in SHRSP were related to altered cGMP activity. We found similar dilatation of cerebral arterioles in WKY and SHRSP in response to nitroglycerin. Thus impaired endothelium-dependent dilatation in SHRSP is not related to alteration of cGMP activity. We speculate that impairment of cerebral vasodilator responses to endothelium-dependent agonists, including vasoactive substances released by platelets, may predispose SHRSP to cerebral ischemia.

Superoxide Dismutase Mimetic Increases Neuronal Nitric Oxide Synthase Influence on Afferent Arteriolar Diameter in Spontaneously Hypertensive Rats

Hypertension ◽  
2000 ◽  
Vol 36 (suppl_1) ◽  
pp. 712-713
Author(s):  
Atsuhiro Ichihara ◽  
Matsuhiko Hayashi ◽  
Nobuhisa Hirota ◽  
Takao Saruta
Keyword(s):  
Nitric Oxide ◽  
Superoxide Dismutase ◽  
Nitric Oxide Synthase ◽  
Superoxide Anion ◽  
Spontaneously Hypertensive Rats ◽  
Neuronal Nitric Oxide Synthase ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Oxide Synthase ◽  
Arteriolar Diameter

P108 This study was designed to determine the influence of increased superoxide anion production in neuronal nitric oxide synthase (nNOS)-dependent regulation of afferent arteriolar diameter in spontaneously hypertensive rats (SHR). Afferent arteriolar diameters of male Wister-Kyoto rats (WKY) and SHR (300-350 g) were assessed in vitro using the blood-perfused juxtamedullary nephron technique and averaged 21.6 ± 1.6 (n = 6) and 18.8 ± 1.2 μm (n = 7); respectively. Superfusion with the superoxide dismutase mimetic, tempol (1, 10, and 100 μmol/L), did not influence afferent arteriolar diameters of WKY, but significantly increased afferent arteriolar diameters of SHR by 20.6 ± 5.5%, 25.2 ± 5.4% and 23.3 ± 4.9%; respectively. In WKY (n = 6), superfusion with the nNOS inhibitor, S -methyl-L-thiocitrulline (L-SMTC; 10 μmol/L), and the NOS inhibitor, N w -nitro-L-arginine (L-NNA; 100 μmol/L), significantly decreased afferent arteriolar diameters (19.6 ± 1.6 μm) by 11.9 ± 3.1% and 21.0 ± 3.9%; respectively. In SHR (n = 7), L-SMTC treatment did not influence afferent arteriolar diameters (21.0 ± 1.5 μm), but L-NNA treatment exerted a significant afferent arteriolar constriction (14.8 ± 3.2%) which was similar to that observed in WKY. Experiments were also performed in the presence of 100 μmol/L tempol. In WKY (n = 6), tempol treatment did not modulate basal afferent arteriolar diameters (21.5 ± 1.2 μm) or afferent arteriolar constrictor responses to L-SMTC (10.6 ± 2.1%) and L-NNA (19.3 ± 3.3%). In SHR (n = 8), tempol treatment significantly increased afferent arteriolar diameters by 22.5 ± 4.3% and enhanced afferent arteriolar constrictor responses to L-SMTC (18.4 ± 2.7%) and L-NNA (31.9 ± 2.6%). However, superfusion with the nitric oxide donor, S -nitroso-N-acetylpenicillamine (10 μmol/L), which exerted a similar afferent arteriolar vasodilation (19.7 ± 3.8%, n = 4), did not influence afferent arteriolar responses to L-SMTC (-2.1 ± 3.1%) or L-NNA (15.1 ± 3.3%). These results suggest that increased superoxide anion inhibits nNOS-dependent regulation of afferent arteriolar diameters in SHR.

Variations in renal arteriolar diameter in deoxycorticosterone acetate-salt hypertensive rats

1990 ◽  
Vol 417 (5) ◽  
pp. 389-393 ◽  
Author(s):  
Akihiro Tojo ◽  
Kenjiro Kimura ◽  
Shinichiro Nanba ◽  
Hiroaki Matsuoka ◽  
Tsuneaki Sugimoto
Keyword(s):  
Hypertensive Rats ◽  
Deoxycorticosterone Acetate ◽  
Acetate Salt ◽  
Arteriolar Diameter
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