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Biomedical subjects

A S Greene

Publications and source records attributed to A S Greene.

At least 37 records · Page 2Linked to original sources
PubMed1998

Laser-Doppler flowmetry utilizing a thinned skull cranial window preparation and automated stimulation.

For several decades, cranial windows have been used to investigate questions relating to cerebral blood flow and its regulation. In general, these techniques have utilized either 'open' cranial windows for the direct observation of the intracranial vasculature, or 'closed' cranial windows in which the skull and dura are removed and replaced with a clear seal, such as a coverslip. Here we describe a method of studying blood flow responses elicited by the physiological stimulus of whisker movement while using a 'thinned skull' cranial window created over the rat whisker-barrel cortex. This method employing an automated whisker stimulator coupled with laser-Doppler flowmetry focused through the thinned skull cranial window, is less invasive than other cranial window techniques, and allows for the study of the effects of stimulation parameters and systemically administered compounds on whisker movement elicited blood flow responses. Automated whisker stimulation and data collection also allow for precise temporal averaging of laser-Doppler measured responses, leading to increased precision in determining the true shape of the evoked blood flow response pattern.

Animals↗
PubMed1998

Localization of the ANG II type 2 receptor in the microcirculation of skeletal muscle.

Only functional studies have suggested the presence of the ANG II type 2 (AT2) receptor in the microcirculation. To determine the distribution of this receptor in the rat skeletal muscle microcirculation, a polyclonal rabbit anti-rat antiserum was developed and used for immunohistochemistry and Western blot analysis. The antiserum was prepared against a highly specific and antigenic AT2-receptor synthetic peptide and was validated by competition and sensitivity assays. Western blot analysis demonstrated a prominent, single band at approximately 40 kDa in cremaster and soleus muscle. Immunohistochemical analysis revealed a wide distribution of AT2 receptors throughout the skeletal muscle microcirculation in large and small microvessels. Microanatomic studies displayed an endothelial localization of the AT2 receptor, whereas dual labeling with smooth muscle alpha-actin also showed colocalization of the AT2 receptor with vascular smooth muscle cells. Other cells associated with the microvessels also stained positive for AT2 receptors. Briefly, this study confirms previous functional data and localizes the AT2 receptor to the microcirculation. These studies demonstrate that the AT2 receptor is present on a variety of vascular cell types and that it is situated in a fashion that would allow it to directly oppose ANG II type 1 receptor actions.

Adrenal Glands↗
PubMed1998

Documentation of angiotensin II receptors in glomerular epithelial cells.

Angiotensin II decreases glomerular filtration rate, renal plasma flow, and glomerular capillary hydraulic conductivity. Although angiotensin II receptors have been demonstrated in mesangial cells and proximal tubule cells, the presence of angiotensin II receptors in glomerular epithelial cells has not previously been shown. Previously, we have reported that angiotensin II caused an accumulation of cAMP and a reorganization of the actin cytoskeleton in cultured glomerular epithelial cells. Current studies were conducted to verify the presence of angiotensin II receptors by immunological and non-peptide receptor ligand binding techniques and to ascertain the activation of intracellular signal transduction in glomerular epithelial cells in response to angiotensin II. Confluent monolayer cultures of glomerular epithelial cells were incubated with angiotensin II, with or without losartan and/or PD-123,319 in the medium. Membrane vesicle preparations were obtained by homogenization of washed cells followed by centrifugation. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis of membrane proteins followed by multiscreen immunoblotting was used to determine the presence of angiotensin II receptor type 1 (AT1) or type 2 (AT2). Angiotensin II-mediated signal transduction in glomerular epithelial cells was studied by measuring the levels of cAMP, using radioimmunoassay. Results obtained in these experiments showed the presence of both AT1 and AT2 receptor types in glomerular epithelial cells. Angiotensin II was found to cause an accumulation of cAMP in glomerular epithelial cells, which could be prevented only by simultaneous use of losartan and PD-123,319, antagonists for AT1 and AT2, respectively. The presence of both AT1 and AT2 receptors and an increase in cAMP indicate that glomerular epithelial cells respond to angiotensin II in a manner distinct from that of mesangial cells or proximal tubular epithelial cells. Our results suggest that glomerular epithelial cells participate in angiotensin II-mediated control of the glomerular filtration barrier.

Angiotensin Receptor Antagonists↗
PubMed1998

Life and death in the microcirculation: a role for angiotensin II.

OBJECTIVE: Angiotensin II (ANGII) plays a critical role in the maintenance of the microcirculation and in the anatomical loss of microvessels (rarefaction) that occurs in low renin forms of hypertension and in animals fed a high-salt diet. Elevations in sodium intake can trigger a series of hemodynamic and hormonal responses culminating in a substantial rarefaction of small arterioles and capillaries in both normal and reduced renal mass hypertensive rats. METHODS: Immunohistochemistry, Northern blot, and reverse transcription-polymerase chain reaction (RT-PCR) analysis of microdissected blood vessels were used to localize ANGII receptors in the microcirculation. Chronic infusion of ANGII and other physiologic and pharmacologic manipulations of the reninangiotensin system in rats was combined with morphologic and mathematical analysis of the network architecture. RESULTS: We have shown that rarefaction of the microcirculation can cause an increase in total peripheral resistance, reduced tissue perfusion, decreased oxygen delivery, and impaired organ function. Although the mechanisms by which this occurs are not well understood, a number of key observations point to a role for the renin-angiotensin system in this effect. First, ANGII infused systemically at subpressor levels, or locally into the skeletal muscle interstitium, can induce significant microvessel growth. Second, localization of ANGII receptor proteins by immunohistochemistry and Western blotting and RNA localization by RT-PCR confirm the presence of AT1 receptors, which are growth-stimulatory, and AT2 receptors, which are growth-inhibitory in the microcirculation. Third, maintenance of ANGII at normal levels during periods of hypertension or high-salt diet completely eliminates rarefaction. CONCLUSIONS: Taken together, these results support the hypothesis that ANGII acting through AT1- and AT2-receptor mechanisms modulate vessel density during high-salt diet and hypertension.

Angiotensin II↗
PubMed1997

Reversal of microvascular rarefaction and reduced renal mass hypertension.

This study examined the microcirculatory and renin-angiotensin system changes following the reversal of hypertension in reduced renal mass rats. Nine-week-old Sprague-Dawley reduced renal mass rats were placed on a low or high sodium diet for 4 or 8 weeks or a combination of 4 weeks of high sodium followed by 4 weeks of low sodium. Blood pressure was directly measured during the development of hypertension and its reversal. Plasma renin activity, angiotensin-converting enzyme activity, and angiotensin II concentrations were measured throughout the experiment. The cremaster and hindlimb muscles were removed, and microvascular density was determined by quantitative stereology. Four weeks of high sodium increased blood pressure (152+/-7 mm Hg) and reduced microvessel density (13.7%). Reduced renal mass hypertension was rapidly reversed after the rats were returned to a low sodium diet (124+/-7 mm Hg after 3 days), and microvascular density returned to control levels. After 4 weeks of high sodium, circulating plasma renin activity and angiotensin II fell by 94% and 82%, respectively. Plasma angiotensin-converting enzyme activity was increased after 2 weeks of high sodium but returned to control levels after 4 weeks of high sodium. This study demonstrates that microvascular density is reduced in reduced renal mass hypertensive rats following exposure to high sodium diet and this is associated with a fall in circulating plasma renin activity and angiotensin II levels. Microvascular density can return to normal levels after a reactivation of the circulating renin-angiotensin system. This study provides further evidence for the hypothesis that modulation of the renin-angiotensin system is important in the regulation of microvascular structure.

Analysis of Variance↗
PubMed1997

Suppression of angiotensin-converting enzyme expression and activity by shear stress.

Shear stress caused by the frictional forces of a fluid moving over a cell monolayer is an important regulator of gene expression. In this study, we investigated the effect of shear stress on angiotensin-converting enzyme (ACE) expression and promoter activity in vitro and on local vascular ACE activity in vivo. ACE activity measured in bovine pulmonary artery endothelial (BPAE) cells was reduced by 49.5% after exposure to a shear stress of 20 dyne/cm2 for 18 hours. Short-term shearing (2 hours) elevated ACE activity in BPAE cells, whereas long-term shearing produced a time-dependent reduction in ACE activity by 23.3%, 33.5%, and 48.9% at 8, 12, and 18 hours, respectively. Northern blot analysis revealed that shear stress (20 dyne/cm2 for 18 hours) significantly reduced ACE mRNA expression by 82%. To determine the mechanism of ACE activity and message reduction, the effect of shear on transcriptionally related events was determined in a rabbit aortic endothelial cell line (W3LUC) stably transfected with 1.3 kb of a rat ACE promoter/luciferase construct. Different shear stress magnitudes (5 to 20 dyne/cm2) caused suppression of luciferase activity by an average of 40.7%. ACE promoter activity was suppressed by 2 hours of shear stress (24.7%) and was further inhibited at time periods > 8 hours. In vivo elevations in shear stress were created by placing a stainless steel clip over a 12-mm region of the rat abdominal aorta. Restriction of vessel diameter increased blood flow velocity and caused reduction in vascular ACE activity by 40%. These studies suggest that elevations in the level of shear stress alter endothelial cell function by suppressing ACE gene and protein expression in vitro and in vivo.

Acetylcholine↗
PubMed1996

Decreases in steady-state muscle performance and vessel density in reduced renal mass hypertensive rats.

In this study we hypothesized that reduced renal mass (RRM) hypertension, which is associated with a chronic reduction in vessel density, could reduce steady-state muscle performance. Vessel density and isometric tetanic force from the in situ gastrocnemius-plantaris-soleus muscle group were studied in age-matched normotensive sham-operated control (HSS) and hypertensive RRM rats on a high-salt (4.0% NaCl) diet (HSRRM) and a low-salt (0.4% NaCl) diet (LSS and LSRRM, respectively). The Achilles tendon was isolated and connected to a force transducer. Peak isometric tension elicited by sciatic nerve stimulation (1/s for 10 min, 50 impulses/s for 330 ms) was not different between the groups. In the LSS, HSS, and LSRRM groups, tension decreased similarly at 3 min to 375 +/- 22, 447 +/- 26, and 424 +/- 21 g/g, respectively. Tension was significantly reduced in the HSRRM group (203 +/- 45 g/g) relative to the LSS, HSS, and LSRRM groups by 3 min. These differences in steady-state tension persisted throughout the remainder of the experiment. Microvessel density, measured by the lectin fluorescence technique, was reduced significantly only in the soleus, plantaris, and medial gastrocnemius of the HSRRM rats. We conclude that RRM hypertension results in reductions in vessel density (rarefaction) that are associated with decreased steady-state muscle performance.

Animals↗
PubMed1996

Opposing actions of angiotensin II on microvascular growth and arterial blood pressure.

We performed studies to further elucidate the mechanisms of angiotensin II (Ang II)-induced angiogenesis of the microvasculature. Rats were placed on a high salt diet (4% NaCl), and Ang II was infused at a subpressor rate (5 ng/kg per minute) for 3 days. Blood pressure was measured daily for 2 control and 3 infusion days. Microvessel density in the cremaster muscle was measured at the end of the infusion. Vessel density in rats that received subpressor Ang II infusion increased by 12.6% compared with rats that received vehicle infusion. When the angiotensin type 2 (AT2) receptor antagonist PD 123319 was coinfused with Ang II, blood pressure was elevated and vessel density increased above that observed with Ang II infusion alone (23% increase). When the AT1 receptor antagonist losartan was coinfused with Ang II, blood pressure was lower than control and vessel density was reduced compared with the Ang II group but was still greater than control (7.8% increase). In this study, Ang II stimulated angiogenesis in the rat cremaster muscle; this effect was enhanced by AT2 antagonism and inhibited by AT1 antagonism. Ang II infusion at a subpressor dose resulted in a pressor response with AT2 antagonism and a depressor response with AT1 antagonism. This suggests that in the microvasculature, the AT1 receptor mediates angiogenesis and vasoconstriction, and the AT2 receptor mediates an inhibition of angiogenesis and vasodilation.

Angiotensin II↗
PubMed1996

Rapid microvessel rarefaction with elevated salt intake and reduced renal mass hypertension in rats.

To identify the sequence of events associated with the development of reduced vessel density (rarefaction) in hypertension, microvessel density and ultrastructure were assessed in the cremaster muscle of rats subjected to a 75% surgical reduction of renal mass and normotensive sham-operated control rats. Rats with reduced renal mass (RRM rats) and sham-operated rats were then maintained on either a high salt (4.0% NaCl) or a low salt (0.4% NaCl) diet for 3 days. Acute exposure to the high salt diet significantly increased mean arterial pressure in RRM rats but did not affect sham-operated control rats. Quantitative fluorescence microscopy of cremaster muscle whole mounts using rhodamine-labeled Griffonia simplicifolia I lectin revealed substantial rarefaction of microvessels in both RRM hypertensive rats and normotensive sham-operated rats on a high salt diet relative to corresponding control rats on a low salt diet. Confocal microscopy revealed a heterogeneous distribution of microvessels in RRM rats on a high salt diet, with some areas largely devoid of vessels. RRM and sham-operated rats on a high salt diet both exhibited changes in arteriolar ultrastructure, which included a loss of basement membranes and a dissociation of the endothelial and smooth muscle components of the vascular wall, resulting in a loss of vessel integrity. These observations demonstrate that a rapid loss of microvessels can occur not only in rats with RRM hypertension but also in normotensive rats on a high salt diet. This loss of microvessels results from structural alterations, which differ from the degenerative processes associated with microvascular rarefaction in rats with chronic RRM hypertension.

Animals↗
PubMed1995

A computerized method for determination of microvascular density.

Currently accepted stereological methods for vascular density measurements involve manual counting of labeled vessels with a grid image overlay and determination of vessel-grid intersections. This method both is tedious and may be prone to error; therefore, our laboratory has developed a method for computer-automated determination of microvascular density using digital image processing techniques. An image of the microvasculature is acquired using computer videomicroscopy. The image is processed in three general steps, involving (1) background correction, (2) thresholding of the gray level image to create a binary image, and (3) processing of the binary image using erosion, dilation, and skeletonization algorithms. Testing of this procedure was performed on 328 typical images of skeletal muscle tissue sections taken from the hindlimb of Sprague-Dawley rats and quantitated by both traditional measures and our new computer method. Results from this comparison reveal that the automated vessel counting is highly correlated (r2 = 0.71) and decreased analysis time from 15 min/image to 30 sec/image when compared with manual counting methods. Our computer-based method also appears to be superior to the traditional method due to the unbiased and nonsubjective nature of determining vessel-grid intersections.

Animals↗
PubMed1995

Hemodynamic and microcirculatory changes during development of renal hypertension.

To study the progression of vessel loss (rarefaction) during the development of hypertension, a plastic window was chronically implanted over the biceps femoralis muscle of reduced renal mass (RRM) and sham-operated control (SOC) rats on a low-salt diet (0.4%). Blood pressure was measured directly via a catheter implanted in the femoral artery, and tissue blood flow was measured by laser-Doppler flowmetry before and after local topical application of sodium nitroprusside. Measurements were made on the control day and after an increase in sodium intake (4.0%) in RRM rats on days 5, 10, 14, 21, and 28. SOC rats on a low-salt diet served as the control group. RRM rats became hypertensive (167 mmHg), and vascular resistance increased after a change in sodium intake. Resting tissue blood flow decreased by 19% by day 28 in RRM but did not change in SOC. Sodium nitroprusside administration reduced vascular resistance to the same level in both RRM and SOC during control and at day 10; however, on all other days, sodium nitroprusside was not able to fully dilate the RRM microcirculation compared with that of SOC. At the same time, microvascular density estimated by computer fluorescence microscopy was decreased by 25% in RRM rats. These studies indicate that the development of RRM hypertension is characterized by a transition from increased tone and vessel closure (functional rarefaction) to anatomic vessel loss (structural rarefaction).

Analysis of Variance↗
PubMed1995

Angiotensin II mediates a sustained rise in nuclear and cytoplasmic calcium via multiple receptor subtypes.

Alterations in nuclear calcium levels in response to angiotensin II (ANG II) may play an important role in the trophic actions of ANG II. This study utilized confocal microscopy and nuclear staining to test the hypothesis that both nuclear and cytoplasmic calcium levels are altered in response to ANG II stimulation of freshly dissociated aortic smooth muscle cells. Cells were loaded with the calcium indicator fluo 3 acetoxymethyl ester, and the calcium response to ANG II stimulation was analyzed over time with a laser-scanning confocal microscope. Additionally, the ratiometric calcium indicator fura 2 acetoxymethyl ester and conventional fluorescence microscopy were used to verify these observations. Results show that basal nuclear calcium exceeds cytoplasmic calcium in these cells. Stimulation by ANG II induces a sustained rise (separate from the rapid transient) in both nuclear and cytoplasmic calcium in excess of 20 min in duration. This rise was blockable by either the AT1 receptor antagonist DuP-753 or by the AT2 antagonist PD-123319. Thus ANG II stimulates a sustained rise in nuclear calcium by a mechanism that necessitates activation of both AT1 and AT2 receptors.

Angiotensin II↗
PubMed1994

Hypoxia increases the activity of Ca(2+)-sensitive K+ channels in cat cerebral arterial muscle cell membranes.

The cellular mechanisms mediating hypoxia-induced dilation of cerebral arteries have remained unknown, but may involve modulation of membrane ionic channels. The present study was designed to determine the effect of reduced partial pressure of O2, PO2, on the predominant K+ channel type recorded in cat cerebral arterial muscle cells, and on the diameter of pressurized cat cerebral arteries. A K(+)-selective single-channel current with a unitary slope conductance of 215 pS was recorded from excised inside-out patches of cat cerebral arterial muscle cells using symmetrical KCl (145 mM) solution. The open state probability (NPo) of this channel displayed a strong voltage dependence, was not affected by varying intracellular ATP concentration [(ATP]i) between 0 and 100 microM, but was significantly increased upon elevation of intracellular free Ca2+ concentration ([Ca2+]i). Low concentrations of external tetraethylammonium (0.1-3 mM) produced a concentration-dependent reduction of the unitary current amplitude of this channel. In cell-attached patches, where the resting membrane potential was set to zero with a high KCl solution, reduction of O2 from 21% to < 2% reversibly increased the NPo, mean open time, and event frequency of the Ca(2+)-sensitive, high-conductance single-channel K+ current recorded at a patch potential of +20 mV. A similar reduction in PO2 also produced a transient increase in the activity of the 215-pS K+ channel measured in excised inside-out patches bathed in symmetrical 145 mM KCl, an effect which was diminished, or not seen, during a second application of hypoxic superfusion. Hypoxia had no effect on [Ca2+]i or intracellular pH (pHi) of cat cerebral arterial muscle cells, as measured using Ca(2+)- or pH-sensitive fluorescent probes. Reduced PO2 caused a significant dilation of pressurized cerebral arterial segments, which was attenuated by pretreatment with 1 mM tetraethylammonium. These results suggest that reduced PO2 increases the activity of a high-conductance, Ca(2+)-sensitive K+ channel in cat cerebral arterial muscle cells, and that these effects are mediated by cytosolic events independent of changes in [Ca2+]i and pHi.

Animals↗
PubMed1994

Hypertension induced by high salt intake in absence of volume retention in reduced renal mass rats.

Reduction of renal mass (RRM) combined with a high-salt diet results in volume retention, a rise of cardiac output, and hypertension. The present studies were designed to determine whether prevention of volume retention would alter the rise of mean arterial pressure (MAP) in RRM rats given high salt. Rats were studied in a modified metabolic cage to permit continuous determination of total body weight (TBW). In group 1, NaCl was increased from 1 to 14.5 meq/day and delivered isotonically. In group 2, NaCl was increased while TBW was servo-controlled to a constant level. Group 3 was also servo-controlled, but rats received an intravenous infusion of an arginine vasopressin V1 antagonist throughout the study. MAP in group 1 rose 24 mmHg by day 4 of high salt with a parallel increase of TBW of 26 g. In group 2, MAP rose 48 mmHg by day 4 of high salt, while TBW was controlled to within 0.6% of control body weight. With inhibition of vasopressin V1 receptors (group 3), MAP rose 39 mmHg. Nearly equivalent amounts of NaCl were retained in all groups, which was associated with no change of plasma Na in group 1 but an increase of nearly 7 meq/ml in groups 2 and 3. Hematocrit fell nearly 9% in groups 2 and 3 compared with a 4% reduction in group 1. The results suggest that under conditions where net retention cannot occur, high salt intake increases MAP by an osmotically driven fluid transfer from cells, which results in an even greater expansion of blood volume.(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗
PubMed1993

Imaging system for three-dimensional mapping of cerebrocortical capillary networks in vivo.

A personal computer-based image analysis system was developed for the three-dimensional mapping of cerebrocortical capillary networks from intravital video recordings. Capillary circulation in the parietal cortex of anesthetized rats was visualized to 70 microns depth using a closed cranial window preparation and epi-fluorescent, intensified video microscopy. The circulation was video recorded during slow (0.1 micron/frame) scanning of the focal plane (depth of field = 10 microns) through regions of interest. Capillary networks were traced from still video images of several microscope fields recorded at different X, Y, and Z stage coordinates. The length of vessel segments from five networks ranged between 10 and 178 microns and was best approximated by the Gamma distribution. Vessel diameter (2.5 to 8.7 microns) was best fitted by the lognormal distribution. A specific capillary network contained 51 segments and five anastomosing loops with circumferences between 575 and 1226 microns. Velocity of fluorescently labeled red blood cells ranged from 0.77 to 2.22 mm/sec within the capillary loops. The study demonstrates the feasibility of reconstructing capillary networks from intravital video recordings as deep as 70 microns within the cerebral cortex and finds an anastomosing pattern and heterogeneous red blood cell velocity in the capillary network.

Anastomosis, Surgical↗
PubMed1993

Breathing periodicity in intact and carotid body-denervated ponies during normoxia and chronic hypoxia.

Periodic oscillations in pulmonary ventilation (VI), tidal volume (VT), and inspiratory and expiratory times (TI and TE) were studied during normoxia (arterial PO2 = 95 Torr) and 48 h of hypoxia (arterial PO2 = 40-50 Torr) in awake intact (n = 8) and carotid body-denervated (CBD; n = 8) ponies. Periodic oscillations were identified by fast-Fourier transformation of breath-by-breath data and quantitated by determining the power ratio of significant periodic oscillations to total power of data sequence. Periodic oscillations of 0.063-0.500 cycles/breath were observed in all parameters during both normoxia and hypoxia. During normoxia, CBD accentuated periodicity of VT (P < 0.02) and VI (P < 0.01) but did not change TI or TE periodicity (P > 0.05). These findings suggest that carotid chemoreceptors serve to stabilize breathing (i.e., decrease periodicity) during normoxia, conceivably because of their shorter response time compared with that of central chemoreceptors. During certain periods of hypoxia, periodicity of VT and VI was significantly (P < 0.05) increased in intact ponies. The response to hypoxia in CBD ponies was variable, with VI periodicity significantly (P < 0.05) increasing, decreasing, or unchanging. Because some CBD ponies significantly changed their periodicity during hypoxia compared with normoxia, we conclude that carotid chemoreceptors are not requisite for hypoxia-induced changes in periodic breathing. In addition, our observations in both groups of ponies during normoxia and hypoxia suggest that multiple mechanisms may lead to periodic oscillations in breathing.

Animals↗
PubMed1993

Insulin does not reduce forearm alpha-vasoreactivity in obese hypertensive or lean normotensive men.

Evidence supports the hypothesis that an impaired capacity of insulin to antagonize norepinephrine-induced vasoconstriction increases alpha-adrenergic tone in overweight young men with insulin resistance and mild hypertension. Therefore, the effects of regionally infused insulin at 100 microU/mL on forearm blood flow (milliliters per deciliter per minute) and responses to norepinephrine were measured in seven obese hypertensive and eight lean normotensive men younger than 45 years old. The obese hypertensive men were hyperinsulinemic and insulin resistant compared with the normotensive men, as evidenced by abnormal values for fasting insulin (15.5 +/- 1.6 versus 7.2 +/- 0.8 microU/mL, P < .001), the insulin area under the curve in response to a 2-hour oral glucose tolerance test (12.0 +/- 1.5 versus 6.7 +/- 1.1 mU x min/dL, P < .01), and the disappearance rate of glucose during a 15-minute insulin tolerance test (2.7 +/- 0.3 versus 4.1 +/- 0.3 mg%/min, P < .05). The logarithm of the norepinephrine EC50 was not significantly different in obese hypertensive men (mean, 95% confidence interval: -8.15, -8.42 to -7.87) versus lean normotensive men (-7.91, -8.23 to -7.59). The 2-hour regional insulin infusion at 100 microU/mL did not significantly alter the EC50 for norepinephrine in either group. Insulin at this concentration induced significant and similar increases of forearm blood flow in the hypertensive and normotensive groups (1.7 +/- 0.4 versus 1.7 +/- 0.6 mL/100 mL per minute, P = NS). At approximately 100 microU/mL, insulin does not antagonize norepinephrine-induced vasoconstriction in the forearm circulation of either obese hypertensive or lean normotensive men.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗