PubMed Health⌕ Search

Biomedical subjects

J P Gilmore

Publications and source records attributed to J P Gilmore.

At least 19 recordsLinked to original sources
PubMed1992

In vivo responses of allografted cerebral parenchymal arterioles to ethanol and angiotensin II: effect of calcium channel blockade.

The goals of these studies were to determine: 1) the effect of ethanol and angiotensin II on the diameter of allografted cerebral parenchymal arterioles in vivo, and 2) the effect of the calcium antagonist, verapamil, in modulating the responses of allografted cerebral parenchymal arterioles to ethanol and angiotensin II. Using a chamber technique, neonatal (< 24 hours old) cortical tissue was transplanted onto the cheek pouch of adult hamsters. Eight to thirteen days after allografting, hamsters were anesthetized with sodium pentobarbital (6.0 mg/100 grams i.p.), and allografted cerebral parenchymal arterioles were viewed using intravital microscopy. Diameter of allografted cerebral parenchymal arterioles was measured before (control), during and after topical application of ethanol (0.1%, 0.25%, 0.5%, 1.0%, and 2.0%) and angiotensin II (0.1 and 1.0 ng/ml). Application of ethanol and angiotensin II was repeated after changing the suffusion fluid to one containing verapamil (50 mg/L). We found that ethanol and angiotensin II produced dose-related constriction of allografted cerebral parenchymal arterioles. In addition, verapamil significantly attenuated vasoconstriction produced by ethanol and angiotensin II. Thus, our findings suggest that ethanol and angiotensin II cause constriction of allografted cerebral parenchymal arterioles through a calcium-dependent mechanism.

Angiotensin II↗
PubMed1989

Volume expansion attenuates baroreflex sensitivity in the conscious nonhuman primate.

We examined the effect of intravascular volume expansion (VE) on the arterial baroreflex control of pulse rate (PR) in conscious, chronically instrumented monkeys tethered in their cages. A total of five monkeys was studied after surgical implantation of catheters in the descending aorta, the left atrium, and the internal jugular vein. Mean arterial blood pressure (MABP)-PR stimulus response curves were constructed by decreasing and increasing blood pressure with nitroprusside and phenylephrine, respectively. The data were analyzed with a regression analysis that generated a sigmoid curve and the maximum sensitivity (slope) of the curve. The data were obtained before and after VE with an isotonic isoncotic dextran solution equal to 20% of the estimated blood volume. After VE, the MABP-PR curve shifted to the right at the high blood pressures, and there was a significant decrease in the maximum sensitivity from 5.65 +/- 1.44 for control to 2.14 +/- 0.63 after VE (P less than 0.05). We concluded that VE attenuates the baroreflex control of heart rate in the conscious nonhuman primate.

Animals↗
PubMed1988

Specificity of arginine vasopressin and angiotensin II for microvessels in the hamster cheek pouch after the induction of renovascular hypertension.

The present study was undertaken to determine the specificity of the vasoconstrictor activity to angiotensin II (AII) and arginine vasopressin (AVP) on the microcirculation in normal and renovascular hypertensive states. Ten to fourteen days after the induction of hypertension, Syrian hamsters were anesthetized with pentobarbital sodium, the cheek pouch was exposed, and a plastic chamber was placed in situ so the membrane could be suffused with bicarbonate-buffered Ringer's solution (5% CO2, 95% N2, pH 7.4). Third order arterioles (30-45 micron) were identified for study and vessel diameter was measured using a shearing device. In one group of normotensive and hypertensive hamsters, AII was microapplied to the arteriole before and after adding an AVP antagonist to the suffusate. In a second group of similar hamsters, AVP was microapplied to the arteriole before and after adding an angiotensin II blocker, saralasin acetate, to the suffusate. AVP and AII receptor blockade was documented by observing whether the vasoconstrictor effect of either AVP or AII was abolished. Dose-response curves for either peptide were not altered in the presence of the antagonist to the other peptide; however, they were shifted to the left in the RHT hamsters. Neither AVP nor AII receptor blockade altered control resting arteriolar diameters. Thus, it can be concluded that the microvascular response to both AII and AVP are potentiated in RHT and there are no interactions between either AII or AVP with the receptors of the other peptide in these microvessels in normal or RHT hamsters, indicating a high specificity for each peptide to its vascular receptor.

Angiotensin II↗
PubMed1988

The selective response to adenosine of renal microvessels from hamster explants.

The present study was undertaken to investigate the effect of adenosine on the microvasculature of the hamster kidney and the possibility of angiotensin II mediation. Renal tissue from neonatal hamsters was grafted into the cheek pouch of 33 adult hamsters. Seven to twelve days later the renal microcirculation was studied. Adenosine was tested on the pre- and postglomerular arterioles as well as on cheek pouch arterioles before and after applying an AII antagonist, saralasin. Adenosine dilated the cheek pouch arterioles and constricted the preglomerular arterioles in a dose-dependent manner. Adenosine had no effect on postglomerular arterioles. The renal vasoconstriction persisted as long as adenosine was present. Theophylline reduced the adenosine-mediated vasoconstriction of the afferent arteriole in a dose-dependent manner. These changes were not altered in the presence of saralasin at various doses, one of which was 20-fold greater than that required to abolish the vasoconstrictor response of a test dose of angiotensin II. This study indicates that the adenosine-mediated vasoconstriction of the preglomerular microvessels is not mediated via the renin-angiotensin system but may be a direct effect of adenosine.

Adenosine↗
PubMed1988

Central blood volume and blood pressure in conscious primates.

Conscious intact (I) and sinoaortic-denervated monkeys (SAD) were studied to determine the extent to which high-pressure receptors contribute to the maintenance of arterial blood pressure (BP) when venous return is decreased by hemorrhage (H) or lower body negative pressure (LBNP). In the I animals, mean BP did not decrease significantly until 5% of the estimated blood volume (EBV) was removed, whereas, with sinoaortic denervation, mean BP decreased significantly when less than 2% of EBV was removed. Left atrial pressure (LAP) decreased similarly in both groups of animals. In the I group during LBNP, mean BP did not change significantly, whereas pulse pressure decreased significantly when LBNP was decreased to -5 cmH2O. In the SAD animals, mean BP decreased significantly at an LBNP of -2 cmH2O, and at -5 cmH2O mean BP declined from 134.1 +/- 4 to 102.7 +/- 7 mmHg. LAP decreased similarly in both groups of animals. The data support the view that a nonhypotensive reduction in venous return unloads arterial baroreceptors sufficiently to activate the arterial baroreflex, probably through reductions in pulse pressure. In addition, low-pressure receptors by themselves do not appear to contribute importantly to blood pressure maintenance when venous return is decreased by either LBNP or a nonhypotensive hemorrhage.

Animals↗
PubMed1988

Pentobarbital potentiates natriuretic response to acute volume expansion in monkeys.

We determined the influence of pentobarbital sodium on the renal responses of the monkey to acute intravascular volume expansion. Before volume expansion, the anesthetized animals had a significantly lower blood pressure and creatinine clearance and a significantly higher urine flow and sodium excretion than the conscious animals. After volume expansion with an isotonic, isoncotic, dextran solution, sodium excretion and urine flow increased significantly in both groups of animals. However, both responses were significantly greater in the anesthetized animals. The greater natriuresis in the anesthetized animals was associated with a greater fractional sodium excretion than in the conscious animals. The potentiated response of the anesthetized animal may be the result of a direct renal tubular effect of pentobarbital and/or the result of the anesthetic removing an inhibitory influence on sodium excretion.

Animals↗
PubMed1988

Hypotension produced by vagal block in primates.

In many species, the vagus has been reported to contain afferents that inhibit sympathetic tone. Vagal block (VB) increases blood pressure in both the intact and sinoaortic-denervated (SAD) dog. In the present study, VB was produced in intact and SAD monkeys by infiltrating the vagi with a local anesthetic. This was done in conjunction with blood volume expansion or head-out water immersion. The cardiovascular parameters monitored were heart rate (HR), blood pressure (BP), and left atrial pressure (LAP). VB decreased BP (-13 +/- 2.8 mmHg) in the control group and the SAD animals (-47 +/- 6.7 mmHg) without changing HR. Volume expansion decreased BP in the SAD animals (-6 +/- 3.4) but not in the intact monkeys (1.8 +/- 2.27), whereas HR did not change. Volume expansion after VB increased BP in both the SAD and the intact animals while producing a decrease in HR. Volume expansion caused LAP to increase in all groups (SAD 13.9 +/- 6.3; control VB 11.6 +/- 1.8, control 9.3 +/- 0.89, SAD VB 7.66 +/- 3.46). Immersion in the VB SAD animals increased BP to a greater extent than volume expansion. VB in the monkey must be removing input from peripheral receptors, which maintain sympathetic tone. Because immersion with VB increases BP more than volume expansion with VB, it is concluded that VB causes predominantly venous pooling. Because cardiopulmonary receptors generally inhibit sympathetic tone, it is concluded that those receptors responsible for the observed hypotension are located in the venous system, probably in the chest or the abdominal cavity.

Animals↗
PubMed1988

Angiotensin reactivity in the cheek pouch of the renovascular hypertensive hamster.

Increased reactivity to vasoconstrictor agents and decreased arteriolar luminal diameter have been implicated in the maintenance of hypertension. The same hamster cheek pouch microvessels were tested for angiotensin I (Ang I) and angiotensin II (Ang II) reactivity before and 10 to 14 days after Grollman (two-kidney, one figure-8) or sham operation. Microvascular geometric parameters were measured before and after a maximal vasodilator dose of adenosine. Then maximal vasoconstrictions to Ang I or Ang II were measured: Ang I and Ang II were applied adjacent to arterioles (10(-2)-10(0) pmol) and venules (10(-1) pmol) in 10-microliter aliquots for 1 minute. Blood pressure (178 +/- 11/133 +/- 8 mm Hg) of renovascular hypertensive hamsters was elevated significantly over blood pressure of sham-operated hamsters (120 +/- 11/97 +/- 10 mm Hg). No change was observed in venular geometry or reactivity in renovascular hypertensive hamsters. Arteriolar luminal diameter, wall thickness, wall/lumen ratio, and wall area were not altered in hypertensive hamsters in the normal or vasodilated state; vasodilator capacity was the same in all groups. Conversion of Ang I to Ang II (response to Ang I divided by response to Ang II) for first-order and Third-order arterioles and third-order venules was 74 +/- 5, 79 +/- 3, and 72 +/- 6%, respectively, and was unaltered in renovascular hypertensive hamsters. Although vessel geometry was not altered, there was a significant shift to the left of the Ang I and Ang II dose-response curves of first-order and third-order arterioles, indicating increased sensitivity to these vasoconstrictors.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine↗
PubMed1988

In vivo microscopy of the cerebral microcirculation using neonatal allografts in hamsters.

Studies were performed to characterize the morphology and vascular reactivity of the allografted cerebral microcirculation. Cerebral cortical tissue was allografted into the cheek pouch of the hamster so that cerebral parenchymal vessels could be studied. The vascular morphology was characterized by a large number of looping vessels. The ultrastructural examination indicated viable cerebral tissue containing typical vessels, that is, "tight" junctions, not like those of the cheek pouch. Also, the microvasculature was impermeable to 150, 70, and 20 kDa fluorescein isothiocyanate dextrans. Angiotensin II and norepinephrine caused constriction of the cerebral vessels whereas adenosine caused dilation. Isoproterenol did not affect cerebral arterioles; however, it dilated cheek pouch arterioles. Thus, this preparation provides a satisfactory model for studying the living cerebral microcirculation.

Adenosine↗
PubMed1988

Extravasation of macromolecules and vascular reactivity of microvessels in response to nicotine in the hamster.

The effects of nicotine on the microvasculature were assessed in the hamster cheek pouch and in fetal tissue grafted into the cheek pouch. Transvascular exchange of FITC-dextran (70-150 K) was measured in the cheek pouch of normal hamsters challenged with either intravenous or suffused nicotine, and in streptozotocin-induced, diabetic hamsters challenged for one week with nicotine delivered by a mini-osmotic pump. The effects of nicotine on microvascular diameter were measured in cheek pouch vessels and in grafts 9-12 days after transplantation. Suffused nicotine did not cause leaky site formation or alter dextran clearance from the pouch. Intravenous nicotine had no effect on either of these parameters but potentiated histamine-induced leaky site formation (40%) and clearance (20%); clearance but not leaky site formation was normalized after cessation of nicotine infusion. Chronic nicotine treatment of diabetic hamsters had no effect on either basal or histamine-induced extravasation as monitored by leaky site or clearance measurements. Suffused nicotine had no effect on arteriolar diameter in the cheek pouch, or in renal, pulmonary or atrial allografts. These results indicate that nicotine can modulate histamine-induced extravasation of macromolecules but has no effect on diameter of arterioles in the non-adrenergically innervated vascular beds studied.

Animals↗
PubMed1987

Arteriolar reactivity to pressure stimuli in hamsters with renal hypertension.

The responses to alterations in extravascular pressure were studied in five orders of arterioles in the cheek pouch of normotensive and renal hypertensive hamsters. Renal hypertension was induced by bilateral compression of both kidneys using figure-of-eight ligatures. Ten to 16 days later, hamsters were anesthetized with pentobarbital (6.0 mg/100 g body weight) and a Plexiglas chamber was positioned in the cheek pouch. Chamber pressure, or extravascular pressure, was increased and decreased by +/- 10, 20, and 40 mm Hg, and arteriolar diameters were monitored continuously. The responses at -20 mm Hg and the slope of the linear portion of the chamber pressure-diameter curve (arteriolar gains) were compared between groups for each branching order of arteriole. Arteriolar responses at one chamber pressure and the arteriolar gains were enhanced in third and fourth order arterioles of the renal hypertensive group compared with the normotensive group, and the responses of these small arterioles were greater than those of larger arterioles in both groups. Control diameters of second and third order arterioles were significantly smaller in the renal hypertensive group, while the diameters after adenosine were not different. These results suggest that the enhanced responses of small arterioles in the renal hypertensive group were not related to structural alterations but may be related to an increased reactivity of smooth muscles in these small arterioles to volume expansion, thus a pressure stimulus.

Animals↗
PubMed1987

Hypoxia does not alter angiotensin converting enzyme activity in hamster pulmonary microvessels.

Studies were initiated to investigate the effects of hypoxia on the conversion of angiotensin I (AI) to angiotensin II (AII) in microvessels of the lung. Using the technique of allografting neonatal lung tissue into the cheek pouch of normal hamsters, the microvessels of the lung, pulmonary arterioles, and venules could be visualized and manipulated by direct in vivo microscopy. The microvessels of the lung were studied 7-10 days after allografting by anesthetizing the hamster with pentobarbital (6.0 mg/100 g body weight i.p.) and then preparing the lung tissue for observation. The tissue was suffused with a Ringer's bicarbonate solution bubbled with a normal (20% O2-5% CO2-75% N2) or a low (95% N2-5% CO2) oxygen mixture. After equilibration, a pulmonary arteriole or venule was selected for observation, and the vessel geometry was recorded. Then, a micropipette containing either AI or AII was positioned alongside the vessel, and the agent was delivered continuously for 2 minutes. Lumen diameter was recorded continually for 8-10 minutes. This procedure was repeated until both angiotensins were tested on pulmonary arterioles and venules under conditions of a normal and low oxygen environment. This protocol was repeated on cheek pouch microvessels that did not contain pulmonary allografts. Both AI and AII produced rapid decreases in the lumen diameters of all microvessels tested. This vasoconstriction was greater for AII, and the oxygen environment did not alter the response. Conversion of AI to AII was not altered by the oxygen environment, and the relative conversion was similar in the microvessels of the lung and cheek pouch.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin I↗
PubMed1987

The renal vascular system of the monkey: a gross anatomical description.

This study was conducted on two species of monkeys, Macaca fascicularis and Macaca mulatta, to describe their gross renal vascular morphology. After death, twelve monkeys were perfused with isotonic saline to flush their vascular systems. The monkeys were then perfused either with latex or methyl methacrylate, or both, one into the arterial and the other into the venous system. The results indicated that there were six to eight arterial segments in the monkey kidney, each supplied by a segmental artery. The anterior segments were named apical, upper, middle and lower, while the posterior segments were named posterior-apical, superior, intermediate and inferior. The branching patterns of both the anterior and posterior segmental arteries were classified into one of four types: magistral, cruciate, bifurcating or quadripartite. The renal vein generally collects blood from three or four large intrarenal veins. Peripheral to this, veins accompanied arteries and were given their corresponding names. Despite this juxtaposition of veins and arteries, and the resulting convention in naming vessels, the intrarenal venous system was organised into three regions. Each region was arranged around an anterior and a posterior large intrarenal vein. The various segments of the kidney, as defined by the arterial system, were united by the arcuate veins, which anastomose throughout the corticomedullary region and drain into the large intrarenal veins mentioned above. The gross renal vascular system of the monkey was compared to, and contrasted with, human and canine renal vascular anatomy.

Animals↗
PubMed1986

The renal microvasculature of the monkey: an anatomical investigation.

Twelve monkeys, Macaca fascicularis and Macaca mulatta, were investigated to study their renal microvasculature. After death, all monkeys were perfused with heparinised isotonic saline to flush their vascular systems. The kidneys were then perfused with silicone rubber and examined. The silicone rubber injections allowed description of afferent arterioles and several efferent vascular patterns observed in the subcapsular, midcortical, and inner cortical regions. The medullary vasculature was particularly interesting in that no particular vascular zonation was observable. Silicone rubber injections indicated the existence of vascular bundles that run parallel to one another from outer medulla nearly to the papillary tip. Branching of descending vasa recta into capillaries, or precapillary vessels, occurs frequently and at all levels of the medulla. Ascending vasa recta are formed from the interbundle capillary plexus and from the plexus at the papillary tip. They ascend primarily within vascular bundles to the corticomedullary junction where these vessels may empty into collecting veins or arcuate veins. In addition, many ascending vasa recta penetrate into the cortex where they drain into the proximal third of interlobular veins. The venous drainage of the cortex appears to be regional, in that the area surrounding an interlobular vein generally drains into it directly via venules or small veins. The arterial and venous morphology of the monkey kidney may be important to the monkey's ability to concentrate urine despite the virtual absence of an inner medullary zone. The potential physiological significance of the monkey's microvasculature is discussed extensively and compared with various other mammals.

Animals↗
PubMed1985

Sino-aortic denervation in the monkey.

The aortic arch and carotid sinuses were denervated in eleven monkeys. The monkeys were subjected to four sequential surgeries which involved: (1) implantation of an aortic and left atrial catheter; (2) stripping of the adventitia from the aortic arch; (3) stripping the left carotid sinus and associated vessels; and (4) stripping the right carotid sinus and associated vessels. Blood pressure and pulse rate were recorded 6 days after each surgical procedure. Records were taken over a 6 h period while the monkeys were in their home cages. Baroreceptor denervation was confirmed by: (1) absence of heart rate response to blood pressure changes and (2) an increase in the variability of blood pressure. Veratridine given into the left atrium caused a Bezold-Jarisch reflex both before and after denervation verifying the integrity of the afferent and efferent vagus. Denervation of the baroreceptors resulted in a significant increase in blood pressure when measured from monkeys who were restrained in chairs in the laboratory; however, blood pressure was not significantly elevated in the baroreceptor denervated monkeys while they were tethered in their home cages. It is concluded that denervation of the sino-aortic baroreceptor does not result in a significant increase in systemic blood pressure.

Animals↗
PubMed1985

Renal responses to atrial natriuretic factor during converting enzyme inhibition.

The effect of converting enzyme inhibitor (CEI) on the renal response to atrial natriuretic factor (ANF) was determined in the rat. In the absence of CEI, ANF produced rapid and significant increases in sodium, potassium, calcium, and urine excretions while blood pressure declined transiently. In the presence of CEI, ANF enhanced the excretion of sodium and potassium but not of calcium and urine. The activity of CEI was documented by observing that, in the presence of CEI, the elevation of blood pressure produced by angiotensin I was significantly attenuated. The potentiating effect of CEI on the natriuretic response to ANF supports the hypothesis that converting enzyme may be involved in the metabolism of ANF.

Angiotensins↗
PubMed1985

Renal mechanoreceptors in nonhuman primates.

The present experiments provide the first description of the afferent discharge characteristics of renal mechanosensitive receptors in the nonhuman primate. Twenty-seven single units with mechano-sensitive receptor activity were obtained. Afferent discharge occurred regularly (pulse synchronous) or irregularly (pulse asynchronous) under spontaneous respiration. The activity of pulse synchronous units was increased by partial occlusion of the renal vein and elevation of arterial pressure. Impulse activity decreased or disappeared during bleeding or renal arterial occlusion. The impulse activity of pulse asynchronous units was increased by partial occlusion of the renal vein. The impulse activity of silent units was induced only by partial occlusion of the renal vein. An increase in ureteral pressure (50 mmHg) produced an increase or induced impulse activity in only three of the 27 fibers tested. Compression of the kidney or renal venous occlusion was associated with a decrease in systemic arterial pressure, whereas renal arterial occlusion produced a rise in systemic arterial pressure. An increase in ureteral pressure (50 mmHg) did not produce a change in arterial pressure.

Afferent Pathways↗