Intestinal vasoregulation in spontaneously hypertensive rats

1985 ◽  
Vol 249 (6) ◽  
pp. G786-G791 ◽  
Author(s):  
D. N. Granger ◽  
S. L. Harper ◽  
R. J. Korthuis ◽  
H. G. Bohlen ◽  
P. R. Kvietys
Keyword(s):  
Blood Flow ◽  
Arterial Pressure ◽  
Capillary Pressure ◽  
Vascular Resistance ◽  
Venous Pressure ◽  
Intestinal Blood Flow ◽  
Spontaneously Hypertensive ◽  
Enhanced Sensitivity ◽  
Wistar Kyoto ◽  
Myogenic Factors

The intestinal vascular responses to graded reductions in arterial pressure and elevations in venous pressure were measured in normotensive Wistar-Kyoto (WKY) and spontaneously hypertensive (SHR) rats. Blood flow and capillary pressure were measured in denervated, autoperfused segments of small intestine. Blood flow, capillary pressure, and total vascular resistance were significantly higher in SHR than WKY at the resting mean arterial pressures. Decrements in arterial pressure led to significant reductions in total vascular resistance in WKY but not in SHR. There was a significant tendency for capillary pressure autoregulation in WKY but not in SHR. Increments in venous pressure did not alter vascular resistance in WKY, yet significantly increased total vascular resistance in SHR. The latter effect was due entirely to a rise in precapillary resistance and is consistent with an enhanced sensitivity of the vasculature to myogenic factors. Intestinal blood flow, measured using 15-micro microspheres, was not significantly different between WKY and SHR in innervated preparations. However, in denervated preparations intestinal blood flow was significantly higher in SHR than WKY, indicating that there is a significant neural component to the increased intestinal vascular resistance in SHR.

Mesenteric Blood Flow as Influenced by Progressive Hypercapnia

1956 ◽  
Vol 184 (2) ◽  
pp. 275-281 ◽  
Author(s):  
Eugene W. Brickner ◽  
E. Grant Dowds ◽  
Bruce Willitts ◽  
Ewald E. Selkurt
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Arterial Pressure ◽  
Oxygen Content ◽  
Vascular Resistance ◽  
Pulse Pressure ◽  
Venous Pressure ◽  
Mesenteric Blood Flow ◽  
Initial Tendency ◽  
Elevated Heart Rate

The influence of hypercapnia on mesenteric blood flow was studied in dogs subjected to progressive increments in CO2 content of inspired air produced by rebreathing from a large spirometer. Oxygen content was maintained above 21 volumes %. Although some animals showed an initial tendency for mesenteric blood flow to decrease and arterial pressure to increase in the range 0–5 volumes % of CO2, the usual hemodynamic change in the range 5–16 volumes % was an increase in mesenteric blood flow resulting from decrease in intestinal vascular resistance, accompanied by a decline in arterial pressure. Portal venous pressure was progressively elevated. Heart rate slowed in association with an increase in pulse pressure. The observations suggest that in higher ranges of hypercapnia, CO2 has a direct dilating action on the mesenteric vasculature.

Intestinal capillary filtration in acute and chronic portal hypertension

1988 ◽  
Vol 254 (3) ◽  
pp. G339-G345 ◽  
Author(s):  
R. J. Korthuis ◽  
D. A. Kinden ◽  
G. E. Brimer ◽  
K. A. Slattery ◽  
P. Stogsdill ◽  
...  
Keyword(s):  
Blood Flow ◽  
Portal Hypertension ◽  
Capillary Pressure ◽  
Vascular Resistance ◽  
Interstitial Fluid ◽  
Venous Pressure ◽  
Fluid Pressure ◽  
Lymph Flow ◽  
Interstitial Fluid Pressure ◽  
Capillary Filtration

The impact of acute and chronic portal hypertension on the dynamics of intestinal microvascular fluid exchange was examined in anesthetized, fasted, sham-operated control rats with normal portal pressures (CON), during acute elevations in portal pressure (APH) in control rats, and in rats in which chronic portal hypertension (CPH) was produced by calibrated stenosis of the portal vein 10 days prior to the experiments. Although intestinal blood flow and vascular resistance were not altered by APH in control rats, CPH was associated with an increased intestinal blood flow and reduced intestinal vascular resistance when compared with CON and APH. Intestinal capillary pressure and lymph flow were elevated in APH and CPH relative to control values. However, the increase in both variables was greater in CPH. The capillary filtration coefficient was elevated only in CPH. The transcapillary oncotic pressure gradient was not altered by APH or CPH. Interstitial fluid pressure was increased from -1.1 mmHg in CON to 3.9 mmHg during APH and to 5.0 mmHg in CPH. The results of this study indicate that chronic elevations in portal venous pressure produce larger increments in intestinal capillary pressure and filtration rate than do acute elevations in portal venous pressure of the same magnitude. However, the potential edemagenic effects of elevated capillary pressure in both acute and chronic portal hypertension are opposed by increases in lymph flow and interstitial fluid pressure.

Mechanism of action of vasoconstrictor responses to atriopeptin II in conscious SHR

1985 ◽  
Vol 249 (6) ◽  
pp. R781-R786 ◽  
Author(s):  
R. W. Lappe ◽  
J. A. Todt ◽  
R. L. Wendt
Keyword(s):  
Blood Flow ◽  
Arterial Pressure ◽  
Vascular Resistance ◽  
Regional Blood Flow ◽  
Sympathetic Nerves ◽  
Spontaneously Hypertensive ◽  
Regional Vascular Resistance ◽  
6 Hydroxydopamine ◽  
Renal Vascular ◽  
Renal Sympathetic

Previous studies have demonstrated that infusion of synthetic atriopeptin II (AP II) lowered arterial pressure, reduced regional blood flow, and increased total peripheral and regional vascular resistances in conscious spontaneously hypertensive rats (SHR). This study was designed to examine the mechanism(s) involved in regional vasoconstrictor responses to AP II. In these experiments, hemodynamic actions of AP II were examined in control, 6-hydroxydopamine-treated (chemically sympathectomized), and renal-denervated groups of instrumented conscious SHR. Infusion of AP II (1 microgram X kg-1 X min-1) caused similar reductions in mean arterial pressure in control (-22 +/- 2 mmHg), chemically sympathectomized (-23 +/- 2 mmHg), and renal-denervated (-23 +/- 3 mmHg) SHR. In control SHR, AP II infusion reduced renal (-20 +/- 3%), mesenteric (-26 +/- 2%), and hindquarters (-18 +/- 10%) blood flow and increased regional vascular resistance in all three beds. Chemical sympathectomy prevented the fall in renal blood flow (RBF) and significantly abolished the regional vasoconstrictor responses to AP II infusion. In unilateral renal-denervated groups of SHR, AP II reduced renal vascular resistance (RVR) -11 +/- 3% but failed to alter RBF (-3 +/- 1%) in denervated kidneys. In contrast, RVR increased (20 +/- 7%) and RBF was significantly reduced (-29 +/- 3%) in contralateral-innervated kidneys. This study demonstrated that chemical or surgical destruction of renal sympathetic nerves abolished AP II-induced increases in RVR. These data further indicate that in conscious SHR the regional vasoconstrictor responses to AP II infusion appear to be mediated by increases in sympathetic tone rather than through direct vascular actions of AP II.

scholarly journals Neonatal sympathectomy reduces NADPH oxidase activity and vascular resistance in spontaneously hypertensive rat kidneys

2006 ◽  
Vol 291 (2) ◽  
pp. R391-R399 ◽  
Author(s):  
Torsten Schlüter ◽  
Rita Grimm ◽  
Antje Steinbach ◽  
Gerd Lorenz ◽  
Rainer Rettig ◽  
...  
Keyword(s):  
Blood Flow ◽  
Arterial Pressure ◽  
Nadph Oxidase ◽  
Mrna Expression ◽  
Vascular Resistance ◽  
Oxidase Activity ◽  
Spontaneously Hypertensive ◽  
Nadph Oxidase Activity ◽  
Renal Vascular ◽  
Neonatal Sympathectomy

Neonatal sympathectomy reduces arterial pressure in spontaneously hypertensive rats (SHR). In SHR transplanted with a kidney from sympathectomized SHR, arterial pressure was lower and less Na+ sensitive than in SHR transplanted with a kidney from hydralazine-treated SHR. This study was performed to identify underlying renal mechanisms. Tests for differential renal mRNA expression of nine a priori selected genes revealed robust differences for renal medullary expression of the NADPH oxidase subunit p47phox. Therefore, we investigated the effects of neonatal sympathectomy on renal mRNA expression of NADPH oxidase subunits, NADPH oxidase activity, and renal function. In 10-wk-old sympathectomized SHR fed a 0.6% NaCl diet, medullary p47phox and gp91phox expression was 40% less than in hydralazine-treated SHR. Also, after a 1.8% NaCl diet, medullary p47phox mRNA expression was lower in sympathectomized than in hydralazine-treated SHR. We found lower cortical (−30%, P < 0.01) and medullary (−30%, P < 0.05) NADPH oxidase activities in sympathectomized than in hydralazine-treated or untreated SHR. Glomerular filtration rate, renal blood flow, medullary blood flow, and fractional Na+ excretion in kidney grafts from sympathectomized and hydralazine-treated donors ( n = 8 per group) were similar at baseline and in response to a 20-mmHg rise in renal perfusion pressure. Renal vascular resistance was lower in kidneys from sympathectomized than hydralazine-treated donors (25 ± 2 vs. 32 ± 4 mmHg·min·ml−1, P < 0.05). The results indicate that the sympathetic nervous system contributes to the level of renal NADPH oxidase activity and to perinatal programming of alterations in renal vascular function that lead to elevated renal vascular resistance in SHR.

Pancreatic circulation: intrinsic regulation

1982 ◽  
Vol 242 (6) ◽  
pp. G596-G602
Author(s):  
P. R. Kvietys ◽  
J. M. McLendon ◽  
G. B. Bulkley ◽  
M. A. Perry ◽  
D. N. Granger
Keyword(s):  
Blood Flow ◽  
Arterial Pressure ◽  
Vascular Resistance ◽  
Venous Pressure ◽  
Filtration Coefficient ◽  
Pancreatic Blood Flow ◽  
Capillary Filtration ◽  
Pressure Elevation ◽  
Capillary Filtration Coefficient ◽  
Intrinsic Regulation

The purpose of the present study was to characterize the intrinsic mechanisms involved in the regulation of blood flow and oxygenation in the totally isolated, perfused canine pancreas. Arterial pressure, venous outflow pressure, blood flow, arteriovenous oxygen difference, and capillary filtration coefficient were measured during graded arterial pressure reductions and venous pressure elevation. Reductions in arterial pressure caused pancreatic blood flow and vascular resistance to decrease, whereas venous pressure elevation resulted in a decreased blood flow and increased vascular resistance. The reductions in blood flow produced by arterial and venous pressure alterations were associated with increases in oxygen extraction and capillary filtration coefficient. During the same pressure perturbations, oxygen uptake remained constant between blood flows of 40-100 ml.min-1.100 g-1, yet decreased progressively as blood flow was reduced below 40 ml.min-1.100 g-1. Arterial occlusion resulted in a postocclusive reactive hyperemia, the magnitude of which was related to the duration of occlusion. The findings of this study suggest that intrinsic regulation of pancreatic blood flow can be attributed to both metabolic and myogenic mechanisms. Resistance and exchange vessels both appear to play a role in the regulation of oxygen delivery to the pancreatic parenchyma.

scholarly journals Regional Cerebral Blood Flow in Conscious Stroke-Prone Spontaneously Hypertensive Rats

1984 ◽  
Vol 4 (1) ◽  
pp. 103-106 ◽  
Author(s):  
Kent Fredriksson ◽  
Martin Ingvar ◽  
Barbro B. Johansson
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Arterial Pressure ◽  
Regional Cerebral Blood Flow ◽  
Brain Structures ◽  
Regional Cerebral Blood ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Cerebrovascular Resistance ◽  
Wistar Kyoto

Regional cerebral blood flow (rCBF) was measured autoradiographically with [14C]iodoantipyrine as a diffusible tracer in two strains of conscious normotensive rats (Wistar Kyoto and local Wistar) and in two groups of spontaneously hypertensive stroke-prone rats (SHRSP) with a mean arterial pressure (MAP) below or above 200 mm Hg. In spite of the large differences in arterial pressure, rCBF did not differ significantly between the hypertensive and the normotensive groups in any of the 14 specified brain structures measured. However, rCBF increased asymmetrically within part of the caudate-putamen in two of nine SHRSP with a MAP above 200 mm Hg, indicating a regional drop in the elevated cerebrovascular resistance.

Autoregulation of intestinal blood flow

1960 ◽  
Vol 199 (2) ◽  
pp. 311-318 ◽  
Author(s):  
Paul C. Johnson
Keyword(s):  
Blood Flow ◽  
Arterial Pressure ◽  
Venous Pressure ◽  
Intestinal Blood Flow ◽  
Pressure Reduction ◽  
Interstitial Fluid Volume ◽  
Pressure Flow Studies ◽  
Local Reflex ◽  
Muscle Changes ◽  
Arterial Constriction

Previous experiments have shown that the arterial vessels of the intestine are responsive to changes in portal venous pressure, with pressure elevation causing arterial constriction. The purpose of the present study was to determine whether these vessels respond in a similar fashion to changes in arterial pressure. In 39 pressure flow studies on segments of terminal ileum, resistance decreased with pressure reduction in 72% of the experiments and increased in 28%. The passive increase in resistance with pressure reduction was seen primarily shortly after the surgical procedure was completed. Thus, it appears that the resistance vessels of the intestine are not ordinarily passively distensible with changes in arterial pressure. As a result of this vascular reaction, the influence of arterial pressure on blood flow is at least partially counteracted. The mechanism of this autoregulation of flow is not a local reflex, a change in interstitial fluid volume, or a change in tone of the intestinal muscle. Changes in concentration of aerobic or anaerobic metabolites, and oxygen tension of the tissues were likewise eliminated. It is concluded that autoregulation of intestinal blood flow is a result of the sensitivity of vascular smooth muscle to change in tension (a myogenic response).

Renal and nephron hemodynamics in spontaneously hypertensive rats

1979 ◽  
Vol 236 (3) ◽  
pp. F246-F251 ◽  
Author(s):  
W. J. Arendshorst ◽  
W. H. Beierwaltes
Keyword(s):  
Blood Flow ◽  
Arterial Pressure ◽  
Spontaneously Hypertensive Rats ◽  
Hypertensive Rats ◽  
Mean Values ◽  
Spontaneously Hypertensive ◽  
Arteriolar Resistance ◽  
Single Nephron ◽  
The Mean ◽  
Wistar Kyoto

Renal and nephron hemodynamics were compared between anesthetized, nondiuretic, spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY). Although the mean arterial pressure was higher in SHR than in WKY, 158 VS. 114 mmHg, glomerular filtration rate (GFR) and renal blood flow (RBF) were similar in both groups. So were intrarenal hydrostatic pressures, single nephron GFR (SNGFR), and single nephron blood flow (SNBF). Accordingly, the increased renal vascular resistance (RVR) in SHR was due to predominant preglomerular vasoconstriction. In a second group of SHR, SHR-AC, the femoral arterial pressure was reduced acutely to 114 mmHg by means of aortic constriction above the renal arteries. The mean values for GFR, RBF, SNGFR, SNBF, and intrarenal hydrostatic pressures resembled those in SHR, whereas RVR was less in SHR-AC. These autoregulatory adjustments of RVR were again largely limited to the preglomerular vasculature. Efferent arteriolar resistance was similar in all three groups. We conclude that the enhanced RVR in 12-wk-old SHR is primarily a consequence of a physiological, autoregulatory response of afferent arteriolar resistance to the elevated arterial pressure. Further, RVR in SHR is not fixed and constant but responds appropriately to reductions in renal perfusion pressure.

Atrial extract: hemodynamics in Wistar-Kyoto and spontaneously hypertensive rats

1985 ◽  
Vol 249 (2) ◽  
pp. H265-H271 ◽  
Author(s):  
B. L. Pegram ◽  
M. B. Kardon ◽  
N. C. Trippodo ◽  
F. E. Cole ◽  
A. A. MacPhee
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Vascular Resistance ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Resistance Index ◽  
Organ Blood Flow ◽  
Spontaneously Hypertensive ◽  
Wistar Kyoto ◽  
Atrial Natriuretic

Partially purified low (LMW) and high-(HMW) molecular-weight atrial natriuretic extracts were administered intravenously (540 micrograms protein/kg) to conscious Wistar-Kyoto (WKY) and spontaneously hypertensive (SHR) rats. Both LMW and HMW atrial natriuretic extracts produced an immediate decrease in mean arterial pressure that reached maximum within 5 min and returned to control levels within 30 min. In both strains, cardiac output decreased approximately 14% following administration of LMW. Total peripheral resistance increased only in SHR. Organ blood flow was significantly decreased to skin, brain, heart, kidneys, and splanchnic organs of WKY and to skin, muscle, heart, and splanchnic organs of SHR following administration of LMW. Corresponding increases in organ vascular resistance index were observed in brain, heart, and splanchnic organs of WKY and in skin, heart, and splanchnic organs of SHR. To some extent, the changes in organ blood flow may be a reflection of the decrease in cardiac output induced by LMW. After administration of HMW, no significant changes were observed in cardiac output or total peripheral resistance, although they tended to decrease. Organ vascular resistance was decreased to skin, muscle, brain, and splanchnic organs of SHR. Little difference was observed between WKY and SHR responses to atrial natriuretic extracts. These data indicate that atrial natriuretic extracts have an effect on systemic and regional hemodynamics in conscious rats that differs markedly from those of vasodilators such as nitroglycerin or hydralazine.

Autoregulation of gastric blood flow and oxygen uptake

1981 ◽  
Vol 241 (2) ◽  
pp. G143-G149
Author(s):  
L. Holm-Rutili ◽  
M. A. Perry ◽  
D. N. Granger
Keyword(s):  
Blood Flow ◽  
Oxygen Uptake ◽  
Arterial Pressure ◽  
Vascular Resistance ◽  
Perfusion Pressure ◽  
Venous Pressure ◽  
Oxygen Demand ◽  
Gastric Blood Flow ◽  
Oxygen Extraction ◽  
Sympathetic Denervation

The purpose of this study was to determine whether the ability of the stomach to autoregulate blood flow and oxygen uptake is altered by sympathetic denervation. Blood flow, oxygen extraction, local arterial pressure, and venous pressure were continuously monitored in sympathetically innervated and denervated autoperfused dog stomach preparations. As perfusion pressure was reduced in increments from 120 to 20 mmHg in innervated preparations, blood flow and oxygen uptake decreased while oxygen extraction and vascular resistance increased. Reductions in perfusion pressure in denervated preparations resulted in a decrease in blood flow, oxygen uptake, and vascular resistance, whereas oxygen extraction increased. The ability of the stomach to regulate blood flow and oxygen uptake was significantly improved after denervation, i.e., vascular resistance decreased and oxygen uptake remained relatively constant when arterial pressure was reduced. Oxygen uptake in denervated stomachs was generally higher than that in innervated stomachs. Autoregulation of gastric blood flow therefore appears to be improved by denervation. The better autoregulation observed after denervation may result either from a reduction in sympathetic tone and/or the increase in gastric oxygen demand.

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