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Biomedical subjects

R J Roman

Publications and source records attributed to R J Roman.

At least 109 records · Page 6Linked to original sources
PubMed1993

Relationship between renal perfusion pressure and blood flow in different regions of the kidney.

The present study examined the autoregulation of blood flow in different regions of the renal cortex and medulla in volume-expanded or hydropenic anesthetized rats. Blood flow was measured in the whole kidney by electromagnetic flowmetry, in the superficial cortex with implanted fibers and external probes for laser-Doppler flowmetry, and in the deep cortex and inner and outer medulla with implanted fibers for laser-Doppler flowmetry. At renal perfusion pressure > 100 mmHg, renal blood flow, superficial cortical blood flow, and deep cortical blood flow were all very well autoregulated in both volume-expanded and hydropenic rats. Inner and outer medullary blood flow were also well autoregulated in hydropenia, but blood flow in these regions was very poorly autoregulated in volume-expanded animals. As renal perfusion pressure was decreased below 100 mmHg in volume-expanded and hydropenic animals, renal blood flow, superficial and deep cortical blood flow, and inner and outer medullary blood flow all decreased. The results of these experiments demonstrate that blood flow in both the inner and outer portions of the renal medulla of the kidney is poorly autoregulated in volume-expanded rats but well autoregulated in hydropenic animals. In contrast, blood flow in all regions of the renal cortex is well autoregulated in both volume-expanded and hydropenic animals. These results suggest that changes in resistance in the postglomerular circulation of deep nephrons are responsible for the poor autoregulation of medullary blood flow in volume expansion despite well autoregulated cortical blood flow.

Animals↗
PubMed1993

Influence of the renal medullary circulation on the control of sodium excretion.

Although the role of the renal medullary circulation in the control of urinary concentrating ability is well established, its potential influence on tubular sodium reabsorption is not generally recognized. Nearly 30 years ago, changes in the intrarenal distribution of blood flow were first proposed to contribute to the natriuretic response to volume expansion. However, the lack of reliable methods for studying medullary blood flow limited progress in this area. The recent development of laser-Doppler flowmetry and videomicroscopic techniques for the study of the vasa recta circulation has renewed interest in the role of medullary hemodynamics in the control of sodium reabsorption. Results of these studies indicate that changes in renal medullary hemodynamics alter renal interstitial pressure and the medullary solute gradient and play an important role in the natriuretic response to elevations in renal perfusion pressure, intravenous infusion of saline, and changes in tubular sodium reabsorption produced by vasoactive compounds. What is emerging from these studies is the view that changes in renal medullary hemodynamics represent an important but misunderstood and long-ignored factor in the control of tubular sodium reabsorption.

Animals↗
PubMed1993

Assessment of changes in intrarenal blood flow in conscious rats using laser-Doppler flowmetry.

The present study was designed to develop, for the first time, a method that allows long-term repeated measurements of renal cortical blood flow (CBF) and medullary blood flow (MBF) in conscious unanesthetized rats. The use of fiber-optic probes (0.5 mm diam) for the chronic measurement of renal CBF and MBF was evaluated. Basal renal cortical and medullary laser-Doppler flow (LDF) signals and the responses to intravenous bolus injections of angiotensin II (ANG II, 12.5 ng) were determined every other day for 11 days in conscious Sprague-Dawley rats (n = 9). A recovery period of 5-7 days after surgery was required before stable signals were obtained from the implanted probes. Thereafter, the fiber-optic probes gave reproducible laser-Doppler measurements of CBF and MBF for 11 days. The CBF and MBF responses to intravenous bolus injections of ANG II (12.5 ng) were also constant during this period. Chronic implantation of the fiber-optic probes caused minimal tissue damage and did not significantly alter urine concentrating ability or renal function. These findings suggest that LDF technique with chronically implanted optical fibers provides a new tool for the continuous long-term monitoring of regional blood flow in the kidney of conscious rats.

Angiotensin II↗
PubMed1993

Clofibrate prevents the development of hypertension in Dahl salt-sensitive rats.

We have reported that cytochrome P-450-dependent omega-hydroxylation of arachidonic acid is reduced in microsomes prepared from the renal outer medulla of Dahl salt-sensitive (SS/Jr) rats, but the functional significance of this observation is unknown. The present study examined whether long-term induction of renal fatty acid omega-hydroxylase with clofibrate would alter the development of hypertension in Dahl SS/Jr rats. Dahl SS/Jr rats were placed on a high salt diet (8.0% NaCl) and given either vehicle or clofibrate (80 mg/day) in their drinking water. After 4 weeks of a high salt diet, mean arterial pressure averaged 170 +/- 3 mm Hg in vehicle-treated (n = 17) and 127 +/- 2 mm Hg in clofibrate-treated (n = 19) SS/Jr rats. Clofibrate had no effect on arterial pressure in Dahl salt-resistant rats. The antihypertensive effect of clofibrate was reversible. Mean arterial pressure rose from 131 +/- 4 to 182 +/- 8 mm Hg in the first week after clofibrate treatment (n = 6) was discontinued. Clofibrate had no effect on arterial pressure in SS/Jr rats (n = 9) in which hypertension was already established by feeding the rats a high salt diet for 4 weeks before the study. In clofibrate-treated SS/Jr rats (n = 12), the omega-hydroxylation of arachidonic and lauric acids by renal cortical and outer medullary microsomes was greater than that seen in vehicle-treated rats (n = 9).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Elevated renovascular tone in young spontaneously hypertensive rats. Role of cytochrome P-450.

The present study examined the role of cytochrome P-450 metabolites of arachidonic acid in elevating renal vascular resistance in young spontaneously hypertensive rats (SHR). Differences in vascular tone were assessed in the preglomerular vasculature of 3- to 4-week-old prehypertensive SHR (n = 11) and normotensive Wistar-Kyoto (WKY, n = 10) and Wistar-Lewis (n = 10) rats. Pressure-diameter relations to changes in renal perfusion pressure were compared using the juxtamedullary nephron microvascular preparation perfused in vitro with a physiological salt solution. At a pressure of 60 mm Hg, the basal diameters of the interlobular arteries and proximal and distal afferent arterioles of the SHR averaged 43 +/- 2, 17 +/- 0.3, and 11 +/- 0.4 microns, respectively. The diameters of the interlobular arteries and afferent arterioles were 9% to 14% smaller than those of corresponding vessels in WKY and Wistar-Lewis rats. Addition of P-450 inhibitors, ketoconazole (100 mumol/L) or 7-ethoxyresorufin (1 mumol/L), to the perfusate dilated the afferent arteriole of SHR by 7% to 12%, whereas it increased the diameter by only 0% to 6% in control rats and significantly reduced the differences in the pressure-diameter relation in the preglomerular vasculature of SHR and control rats. Inhibitors of P-450 eliminated the contractile response of afferent arterioles to increases in renal perfusion pressure in all three groups. Removal of calcium from the perfusate eliminated differences in the diameters of the preglomerular vasculature in SHR and normotensive rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1993

20-Hydroxyeicosatetraenoic acid is an endogenous vasoconstrictor of canine renal arcuate arteries.

Recent studies have indicated that renal arteries can produce 20-hydroxyeicosatetraenoic acid (20-HETE) and suggest the potential involvement of a P450 metabolite of arachidonic acid in the myogenic activation of canine renal arteries. In the present study, the effects of 20-HETE on isolated canine renal arcuate arteries were studied. Administration of 20-HETE to the bath or the lumen at concentrations of 0.01-1 microM produced a graded reduction in the diameter of these vessels. In contrast, 19(R)-HETE was a vasodilator, whereas 19(S)-HETE was relatively inactive. The vasoconstrictor response to 20-HETE was not altered by the cyclooxygenase inhibitor indomethacin, endoperoxide/thromboxane receptor antagonist SQ29548, or combined blockade of the cyclooxygenase, lipoxygenase, and P450 pathways using indomethacin, baicalein, and 7-ethoxyresorufin. The response to 20-HETE was associated with depolarization and a sustained increase in the intracellular calcium concentration in renal vascular smooth muscle cells. Patch-clamp studies indicated that 20-HETE significantly reduced mean open time, the open-state probability, and the frequency of opening of a 117-pS K+ channel recorded from renal vascular smooth muscle cells in the cell-attached mode. Microsomes prepared from the renal cortex of dogs produced 20-HETE and 20-carboxyarachidonic acid when incubated with [14C]arachidonic acid. These results indicate that 20-HETE is an endogenous constrictor of canine renal arcuate arteries. The vasoconstrictor response to 20-HETE resembles the myogenic activation of these vessels after elevations in transmural pressure and suggests a potential role for this substance in the regulation of renal vascular tone.

Animals↗
PubMed1993

Cellular and ionic signal transduction mechanisms for the mechanical activation of renal arterial vascular smooth muscle.

Elevations in transmural pressure increase active vascular tone in arteries from most vascular beds, and this myogenic response has been shown to play an important role in the regulation of blood flow in the kidney and other organs. The myogenic response in isolated perfused arteries is associated with depolarization of vascular smooth muscle cells and a rise in intracellular calcium concentration, which is dependent on calcium influx through voltage-sensitive calcium channels. Recent studies have indicated that the myogenic response in renal arteries is associated with the activation of phospholipase C and that arachidonic acid potentiates, whereas inhibitors of cytochrome P-450 and protein kinase C attenuate, this response. Renal arteries produce 20-hydroxyeicosatetraenoic acid (20-HETE) via the cytochrome P-450 pathway when incubated with arachidonic acid. 20-HETE is a potent constrictor of canine and rat renal arterioles. It inhibits K+ channel activity, depolarizes renal vascular smooth muscle cells, and produces a sustained increase in intracellular calcium concentration. In this regard, the vasoconstrictor response to 20-HETE mimics the myogenic activation of renal arteries after elevations in transmural pressure. These studies suggest that the activation of phospholipase C and subsequent increases in the intracellular levels of diacylglycerol, 1,4,5 inositol triphosphate, and cytochrome P-450 metabolites of arachidonic acid may participate in the myogenic response of renal arteries and in the regulation of renal vascular tone.

Animals↗
PubMed1992

Growth of Babesia bigemina parasites in suspension cultures for vaccine production.

An Australian Babesia bigemina vaccine strain was maintained in suspension culture for 40 days. Parasite growth was compared using two tissue-culture flask sizes (25 and 75 cm2), four gas mixes (2%, 2.5%, 3% and 3.5% O2; 5% CO2; and the balance N2) and four packed blood cell (PCV) volumes (7%, 9%, 13% and 18%). The best continuous parasite yields were obtained from suspension cultures in 75-cm2 flasks at a PCV of 13% and gas mixtures of 2%-3% O2, 5% CO2 and the balance N2. Parasite yields per millilitre of culture medium were 3 times those obtained in microaerophilous stationary-phase cultures. The method has thus far been used for 6 months to produce the Australian requirements for live B. bigemina vaccine.

Animals↗
PubMed1992

Sodium activity in the aqueous humor and corneal stroma of the rabbit.

The present study examined the free sodium concentration of the aqueous humor and corneal stroma of both transparent and non-transparent corneas to assess the transendothelial activity gradient for sodium. In the transparent cornea of the adult rabbit, the sodium activity was higher in the aqueous humor than the stroma. This difference in sodium activity would cause water to diffuse down its concentration gradient from stroma to aqueous humor. In this way corneal transparency and the deturgesced state are maintained. Removal of the corneal endothelium in the adult rabbit produced an opaque swollen cornea. Under these conditions the sodium activity was higher in the stroma than the aqueous humor. However, an osmotic gradient was not produced by the Na+ activity gradient because the endothelium was not present to act as a semi-permeable membrane. The corneal endothelium was no longer present to establish and sustain the activity gradient for sodium that is necessary for corneal transparency in the mature rabbit. The transendothelial sodium activity gradient was also measured in 13-day-old rabbits. At this age, the cornea was not yet transparent, nevertheless the free sodium concentration of the aqueous humor was higher than that of the stroma, similar to the adult transparent cornea. This suggests that forces other than the establishment of the proper transendothelial sodium gradient are responsible for the lack of corneal transparency in the young rabbit.

Animals↗
PubMed1992

Spontaneous trait inferences as self-generated primes: implications for conscious social judgment.

The priming literature has documented the influence of trait terms held outside of conscious awareness on later judgment relevant to the primed trait dimension. The present research demonstrated that spontaneous trait inferences can serve as self-generated primes. In Experiment 1, Ss instructed to memorize trait-implying sentences (thus spontaneously inferring traits outside of consciousness) showed assimilation effects in judgment. Ss instructed to form inferences from these sentences (thus consciously inferring traits) showed contrast effects. Experiment 2 demonstrated that these findings were due to semantic activation rather than to a general evaluative response. When evaluatively inconsistent trait constructs were primed, similar patterns of assimilation and contrast were found. Implications for the ubiquitous occurrence of priming through the process of social categorization are discussed.

Adult↗
PubMed1992

Spontaneous flow oscillations in the cerebral cortex during acute changes in mean arterial pressure.

The purpose of this study was to characterize spontaneous oscillations of blood flow in the cerebral cortex of anesthetized rats under control conditions and after mean arterial pressure was altered by various means. Blood flow was monitored using a laser-Doppler flowmeter through the closed cranium. Spontaneous flow oscillations with amplitudes of 14-30% of the mean flow and frequencies of 4-11 cycles/min were recorded when arterial pressures were less than 90 mm Hg. Stepwise hemorrhagic hypotension and unilateral carotid occlusion increased the amplitude of oscillations. The amplitude of oscillations was negatively correlated with the level of mean arterial pressure after manipulation with norepinephrine or sodium nitroprusside. The oscillations were reversibly abolished during dilation of the cerebral circulation by elevating the inspired carbon dioxide content to 5%. The frequency of flow oscillations was very stable during all of the above maneuvers except during the infusion of norepinephrine, which increased the oscillation frequency slightly. The results suggest that flow oscillations are determined primarily by cerebral arterial pressure.

Animals↗
PubMed1992

Mechanism of action of cerebral epoxyeicosatrienoic acids on cerebral arterial smooth muscle.

Microsomal preparations of cat brain incubated with [14C]arachidonic acid produced epoxyeicosatrienoic acids (EETs) that eluted with the same retention times as synthetically prepared 5,6-, 8,9-, and 11,12-EETs. These compounds dilated serotonin-preconstricted, pressurized cat cerebral arteries in a dose-dependent fashion. Epoxide formation was not found in mitochondrial fractions and was dependent on the presence of NADPH. The maximum effects of 8,9-EET and 11,12-EET were greater than those of 5,6-EET. The cellular basis of this vasodilation was further investigated by examining the effects of 8,9-EET and 11,12-EET on K+ channel activity in vascular muscle cells freshly isolated from cat cerebral arteries. Both 8,9-EET and 11,12-EET increased the frequency of opening, mean open time, and open-state probability of a 98-pS K+ channel recorded in the cell-attached mode with 145 mM KCl in the pipette and 4.7 mM KCl in the bath. Blockade of K+ channel activity with tetraethylammonium attenuated the vasodilatory effects of 11,12-EET on serotonin-preconstricted cat cerebral arteries. These results suggest that endogenously formed EETs may participate in local regulation of cerebral blood flow by dilating cerebral arteries through a mechanism that involves activation of K+ channels.

8,11,14-Eicosatrienoic Acid↗
PubMed1992

Renal medullary interstitial infusion of diltiazem alters sodium and water excretion in rats.

The role of renal papillary blood flow in regulation of fluid and electrolyte excretion was examined. The effects of an acute infusion of diltiazem (5 micrograms.kg-1 x min-1) into the renal medullary interstitium on papillary blood flow and sodium and water excretion were studied. Changes of renal blood flow were measured using an electromagnetic flow probe. Cortical and papillary blood flows were measured using laser-Doppler flowmetry. Renal and cortical blood flows were unchanged during medullary interstitial infusion of diltiazem, but papillary blood flow increased 26% (P < 0.05) and remained elevated for 1 h after diltiazem infusion was discontinued. Glomerular filtration rate (GFR) of the infused kidney increased by 21% from a control of 1.0 +/- 0.1 ml.min-1 x g-1 during infusion of diltiazem (P < 0.05), but it returned to control after diltiazem infusion was stopped. Urine flow and sodium excretion increased by 70% (P < 0.05), and fractional sodium excretion rose from 1.5 +/- 0.2 to 2.4 +/- 0.3% of the filtered load during the hour after diltiazem infusion. Renal blood flow, cortical and papillary blood flow, GFR, urine flow, and sodium excretion in the 0.9% sodium chloride vehicle-infused kidney were not significantly altered during the experiment. Intravenous infusion of the same dose of diltiazem (5 micrograms.kg-1 x min-1) increased GFR by 22%, but had no effect on urine flow and sodium excretion. These results indicate that renal medullary interstitial infusion of diltiazem selectively increased renal papillary blood flow, which was associated with an increase of sodium and water excretion.

Animals↗
PubMed1992

Effect of kinin receptor antagonists on renal hemodynamic and natriuretic responses to volume expansion.

The role of kinins in the natriuretic and papillary blood flow (PBF) responses to intravenous administration of 0.9% sodium chloride solution equal to 5% of body weight over 30 min was evaluated using a B1-kinin receptor antagonist (des-Arg9, [Leu8]bradykinin, 2.5 micrograms/min i.v.) and a B2-kinin receptor antagonist (D-Arg, [Hyp3,Thi5,8,D-Phe7]bradykinin, 2.5 micrograms/min i.v.). In control rats, PBF increased 43 +/- 5% after the volume expansion with saline. Administration of the B1-kinin receptor antagonist had no significant effect on basal PBF or the rise in PBF produced by volume expansion. In contrast, administration of the B2-kinin receptor antagonist decreased basal PBF by 18 +/- 3% and prevented the rise in PBF during volume expansion. Urine osmolality was lower in the rats treated with the B1-antagonist and higher in rats infused with the B2-kinin antagonist than in control animals after volume expansion (587 +/- 47 and 1,082 +/- 83 vs. 907 +/- 124 mosmol/kgH2O, respectively). The initial natriuretic response during the first 30 min after volume expansion was similar in rats given vehicle or the kinin antagonists. However, cumulative sodium excretion over the 2-h course of the experiment was significantly lower in the rats given the B2-receptor antagonist than in control rats (92 +/- 7 vs. 101 +/- 9% of the administered load). The B1-kinin receptor antagonist had no effect on cumulative sodium excretion; however, glomerular filtration rate was 30% lower in rats receiving the B1-antagonist than in control rats after volume expansion.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Normalization of pressure-natriuresis by nisoldipine in spontaneously hypertensive rats.

This study examined whether the calcium antagonist nisoldipine can shift the relations between sodium excretion, papillary blood flow, renal interstitial pressure, and renal perfusion pressure toward lower pressures in spontaneously hypertensive rats. Mean arterial pressure decreased similarly by 9% and 12% in Wistar-Kyoto and spontaneously hypertensive rats after nisoldipine (0.5 microgram/kg bolus + 0.017 microgram/kg/min). Urine flow and sodium excretion increased by 35% and 24% in Wistar-Kyoto rats after nisoldipine. In contrast, urine flow and sodium excretion rose by 121% and 132% in spontaneously hypertensive rats, and fractional sodium excretion rose from 1.9 +/- 0.3 to 4.2 +/- 0.4%. Control sodium excretion, papillary blood flow, and renal interstitial pressure were significantly lower in spontaneously hypertensive rats than in Wistar-Kyoto rats when compared at similar renal perfusion pressures. Sodium excretion, papillary blood flow, and renal interstitial pressure all increased in spontaneously hypertensive rats after nisoldipine, whereas it had no effect on papillary blood flow or renal interstitial pressure in Wistar-Kyoto rats. The relations among sodium excretion, papillary blood flow, renal interstitial pressure, and renal perfusion pressure were shifted toward lower pressures in spontaneously hypertensive rats given nisoldipine and became similar to those seen in Wistar-Kyoto rats. These results indicate that nisoldipine normalizes the relations among sodium excretion, renal interstitial pressure, papillary blood flow, and renal perfusion pressure in spontaneously hypertensive rats perhaps by correcting the defect in renal medullary perfusion associated with resetting of pressure natriuresis in this model of hypertension.

Animals↗
PubMed1992

Role of nitric oxide in renal papillary blood flow and sodium excretion.

Renal medullary interstitial infusion of NG-nitro-L-arginine (120 micrograms/hr, n = 7) decreased papillary blood flow to 71 +/- 5% of control without altering outer cortical flow. Before NG-nitro-L-arginine infusion, interstitial acetylcholine administration (200 micrograms/hr) increased cortical and papillary blood flow to 134 +/- 6% and 113 +/- 2% of control, respectively. After NG-nitro-L-arginine administration, the vasodilator response to acetylcholine was abolished. In clearance experiments, renal medullary infusion of NG-nitro-L-arginine (120 micrograms/hr, n = 7) significantly decreased total renal blood flow by 10%, renal interstitial fluid pressure by 23%, sodium excretion by 34%, and urine flow by 39% without altering glomerular filtration rate, fractional sodium and water excretion, blood pressure, or urine osmolality. These data indicate that selective inhibition of nitric oxide in the renal medullary vasculature reduces papillary blood flow, which is associated with decreased sodium and water excretion. We conclude that nitric oxide exerts a tonic influence on the renal medullary circulation.

Animals↗
PubMed1992

Nitric oxide modulates vascular tone in preglomerular arterioles.

Blockade of nitric oxide reduces renal blood flow, but the site or sites at which nitric oxide alters renal vascular resistance are unknown. The effects of N omega-nitro-L-arginine (100 microM), an inhibitor of nitric oxide synthesis, on the pressure-diameter relation of renal arterioles was studied using a rat juxtamedullary microvascular preparation perfused in vitro with a physiological salt solution containing 5% albumin. The basal diameters of the main arcuate and interlobular arteries and the proximal and distal afferent arterioles averaged 438 +/- 26, 64 +/- 4, 30 +/- 1, and 20 +/- 1 microns, respectively, at a perfusion pressure of 80 mm Hg. The diameters of the arcuate and interlobular arteries increased by 14 +/- 2% and 7 +/- 2%, whereas the proximal and distal afferent arterioles decreased by 3 +/- 1% and 7 +/- 2% when perfusion pressure was elevated to 160 mm Hg. Nitro-arginine had no effect on the basal diameters of arcuate and interlobular arteries. Nitro-arginine reduced the diameters of afferent arterioles by 7 +/- 2% at all perfusion pressures studied. Nitro-arginine increased active vascular tone in the interlobular artery and afferent arterioles and enhanced autoregulation of glomerular capillary pressure. L-Arginine (1 mM), the precursor to nitric oxide production, reversed the effects of nitro-arginine. These findings suggest that nitric oxide modulates vascular tone of the interlobular artery and afferent arterioles of deep nephrons and influences the ability of the preglomerular vasculature to autoregulate glomerular capillary pressure.

Animals↗