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Biomedical subjects

E M Hasser

Publications and source records attributed to E M Hasser.

53 records · Page 3Linked to original sources
PubMed1989

Central effect of angiotensin II on baroreflex regulation in conscious rabbits.

Central effects of angiotensin II (ANG II) on arterial baroreflex control of renal sympathetic nerve activity (RSNA) and heart rate (HR) were examined in conscious rabbits. Intravenous infusions of ANG II (5-320 ng.kg-1.min-1) significantly reduced the baroreflex inhibition of HR compared with phenylephrine (PE) (0.5-16 micrograms.kg-1.min-1), whereas reflex inhibition of RSNA was unaltered. Background intravenous infusions of ANG II did not alter the baroreflex responses of RSNA nor HR to increases (with PE) or decreases in mean arterial pressure (with nitroglycerin or inferior vena cava occluder). When ANG II was infused into the vertebral artery (VA) the integrated pressor response was greater than intravenous infusions. Progressive VA infusions of ANG II resulted in a significantly blunted baroreflex inhibition of HR compared with intravenous infusions, whereas the reflex inhibition of RSNA was identical between VA and intravenous infusions. These results suggest that ANG II produces central pressor effects via a hindbrain site and reduces baroreflex inhibition of HR without altering baroreflex inhibition of RSNA.

Angiotensin II↗
PubMed1988

Osmotically released vasopressin augments cardiopulmonary reflex inhibition of the circulation.

Exogenous arginine vasopressin (AVP) has been shown to augment the inhibitory influence of arterial and cardiopulmonary baroreflexes. This study examined the influence of osmotically released AVP on the inhibitory responses to activation of cardiopulmonary receptors by administration of veratrum alkaloids. Three groups of conscious dogs, with carotid sinus intact, with prior sinoaortic denervation (SAD), and with prior lesion of the area postrema (AP), were instrumented for monitoring arterial pressure and heart rate and with left circumflex coronary artery or left atrial catheters for administration of veratrum alkaloids. Conscious dogs were administered veratridine (0.5-1.0 microgram.kg-1.min-1) under control conditions, after infusion of hypertonic saline (HS, 6% NaCl), and after HS in the presence of the AVP vascular (V1) receptor antagonist. In carotid sinus-intact dogs, veratridine reduced arterial pressure (-10 +/- 0.4 mmHg). After HS infusion, the depressor response to veratridine was significantly greater (-18 +/- 0.8 mmHg). The enhanced depressor response during HS infusion was prevented by administration of the AVP antagonist (-8 +/- 0.6 mmHg). Responses to veratrum alkaloids in SAD dogs were similar. In AP-lesioned animals, the depressor effects of veratridine (-9 +/- 0.5 mmHg) were similar to intact animals. However, the response to veratridine during HS was not altered (-9 +/- 0.8 mmHg) in AP-lesioned dogs. Results suggest that osmotically stimulated AVP augments the inhibitory effects of cardiopulmonary reflexes and that this effect is mediated through the area postrema via the V1 receptor.

Animals↗
PubMed1988

Neurogenic and humoral factors maintaining arterial pressure in conscious dogs.

This study examined the contribution of each primary pressor system to resting arterial pressure and the ability of each to maintain pressure in the absence of the other systems in conscious dogs. In dogs with intact carotid sinus baroreflexes, ganglionic blockade (GB) reduced blood pressure by 13 +/- 3 mmHg, whereas blockade of the renin-angiotensin (RAS) and arginine vasopressin (AVP) systems did not significantly alter arterial pressure. After removal of the other two systems, the depressor response to blockade of the sympathetic nervous system (SNS) with hexamethonium and atropine was significantly augmented (-33 +/- 3 mmHg), whereas captopril (CAP) blockade of the RAS reduced pressure 14 +/- 4 mmHg, and AVP blockade decreased pressure 12 +/- 2 mmHg. In sinoaortic-denervated (SAD) dogs, the SNS exhibited a greater contribution (28 +/- 4 mmHg) to resting pressure compared with intact, and the role of the RAS (10 +/- 2 mmHg) was also augmented, whereas the effects of AVP blockade were unaltered. Effects of GB and CAP were unaltered after blockade of the other systems in SAD animals, whereas the depressor response to AVP antagonist (-13 +/- 2 mmHg) was significantly augmented. Results indicate the SNS is the primary pressor system in resting intact or SAD conscious dogs, whereas the RAS also contributes to resting blood pressure in SAD animals. The ability of the SNS alone to maintain arterial pressure after acute removal of the other systems is also significantly greater than that of AVP or the RAS.

Animals↗
PubMed1987

Vagal cold block in area postrema-lesioned dogs: interaction of vasopressin and sympathetic nervous system.

This study evaluated the interaction between arginine vasopressin (AVP) and the sympathetic nervous system (SNS) during bilateral vagal cold block (BVB) and the arterial baroreflex response to phenylephrine (PE) and exogenous AVP in conscious sham-operated (sham) and area postrema (AP)-lesioned mongrel dogs. The hemodynamic responses to ganglionic blockade (GB) and the vascular (V1) AVP receptor antagonist [d(CH2)5Tyr(Me)]AVP (AVPX) were similar in sham and AP-lesioned dogs. Elimination of the AVP pressor system by AVPX in sham dogs did not alter the pressor response to BVB, whereas subsequent blockade of the SNS by GB abolished the response to BVB. When GB was first imposed, however, it alone eliminated only 55% of the pressor response to BVB, whereas subsequent AVPX eliminated the remaining pressor response to BVB. In contrast, in AP-lesioned dogs, AVPX alone substantially reduced the pressor response to BVB. Additionally, the apparent contribution of each pressor system to the response to BVB was not enhanced in the absence of the other system, as had been seen in the sham dogs. These data indicate that during interruption of vagal afferent activity, reflexly released AVP appears to limit the reflex activation of the SNS. This interaction of AVP with the cardiopulmonary reflex is eliminated following ablation of the area postrema. Infusion studies with PE and AVP indicate that AVP significantly augments baroreflex inhibition of heart rate when compared with PE. Ablation of the area postrema did not alter the arterial pressure-heart rate relationship obtained with PE but eliminated the augmented response to AVP.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Inhibition of renal sympathetic nervous activity by area postrema stimulation in rabbits.

This study investigated the effect of chemical and electrical stimulation of the area postrema on renal sympathetic nerve activity (RSNA), arterial pressure, and heart rate in urethan-anesthetized rabbits. Electrical stimulation of the area postrema at 2, 5, 10, 20, 40, and 80 Hz using constant currents of 7.5, 15, and 30 microA (pulse duration = 0.3 ms, train duration = 5 s) produced progressive decreases in RSNA and heart rate, with no consistent change in arterial pressure. To control for electrical activation of fibers of passage in or near the area postrema, L-glutamate was injected into the area postrema using glass micropipettes. Micropressure injection of L-glutamate (10 mM) in volumes of 5-10 nl produced rapid decreases in RSNA averaging 27 +/- 5% (P less than 0.05) accompanied by a small bradycardia. The effects of electrical stimulation of the area postrema, but not the adjacent nucleus tractus solitarius, were totally eliminated by micropressure injection of kainic acid (40 ng in 40 nl) into the area postrema. During continuous electrical stimulation of the area postrema using parameters that produced small decrements in RSNA and heart rate, the slope of the line relating baroreflex inhibition of RSNA to increases in arterial pressure during graded infusions of phenylephrine was significantly enhanced (-6.77 +/- 1.30 vs. -3.81 +/- 0.66% RSNA/mmHg). These data are consistent with the hypothesis that activation of neurons in the area postrema results in an inhibition of RSNA. Furthermore, stimulation of the area postrema augments baroreflex inhibition of RSNA during increases in arterial pressure with phenylephrine.

Animals↗
PubMed1987

Interaction of vasopressin with area postrema during volume expansion.

Effects of arginine vasopressin (AVP) on inhibition of renal sympathetic nerve activity (RSNA) during activation of cardiopulmonary reflexes by volume expansion were examined in conscious sinoaortic-denervated rabbits. The role of the area postrema in mediating these effects was also evaluated in rabbits subjected to area postrema lesion. Animals were subjected to 12% volume expansion with whole blood alone or during infusion of AVP (0.6 mU . kg-1 . min-1). Volume expansion in area postrema-intact animals caused a progressive reflex inhibition of RSNA (maximum = -36.5 +/- 3.3% delta RSNA). Vasopressin infusion did not significantly alter resting arterial pressure, right atrial pressure, heart rate, or RSNA. However, maximum inhibition of RSNA during volume expansion (-62.6 +/- 3.2% delta RSNA) was significantly augmented during AVP infusion, and the augmentation was reversed by a specific vascular (V1) AVP receptor antagonist. Vagotomy eliminated RSNA responses to volume expansion with or without AVP. In area postrema-lesioned animals, the RSNA response to volume expansion was similar to that of intact animals (-31.8 +/- 2.3% delta RSNA). However, AVP did not augment the RSNA response to volume expansion in lesioned animals (-30.4 +/- 2.5% delta RSNA). Thus exogenous AVP augmented cardiopulmonary reflex-mediated inhibition of RSNA due to volume expansion. This effect appeared to be mediated by the V1 AVP receptor and to require the presence of an intact area postrema.

Animals↗
PubMed1987

Baroreflex control of renal nerve activity in conscious animals.

This study quantitates the effect of three different doses of vasopressin on the arterial baroreflex control of renal sympathetic nerve activity and heart rate. The lowest dose of vasopressin (0.4 mU/kg X min), which had no significant effect on resting mean arterial pressure, heart rate, or renal sympathetic nerve activity, increased the inhibitory influence of arterial baroreflexes on renal sympathetic nerve activity in response to an increase in pressure. During infusions of higher doses of vasopressin (1.5 and 3.0 mU/kg X min), which significantly decreased resting heart rate and renal sympathetic nerve activity but had no significant effect on mean arterial pressure, the mean arterial pressure-renal sympathetic nerve activity relation showed a significant decrease in maximum renal sympathetic nerve activity when compared with control. The highest dose of vasopressin resulted in a significant shift of the relation to the left toward lower pressures and in a decrease in maximum gain. The relation exhibited a parallel shift toward lower pressure, with no change in gain, at the higher dose of vasopressin. Based on these results, we conclude that vasopressin exerted a dose-related effect on arterial baroreflex such that lower doses of vasopressin may sensitize the central baroreflex neurons to afferent input, while the higher doses of vasopressin caused direct excitations of these neurons, resulting in a reduction in resting sympathetic outflow.

Animals↗
PubMed1985

Role of vasopressin and sympathetic nervous system during hypertonic NaCl infusion in conscious dog.

The contribution of arginine vasopressin (AVP) and the sympathetic nervous system to the pressor response elicited by hypertonic NaCl infusion was investigated in conscious dogs with intact carotid sinus baroreceptors or in dogs subjected to chronic sinoaortic baroreceptor denervation (SAD). Infusion of 6% NaCl at 0.05 ml X kg-1 X min-1 for 60 min increased plasma osmolality an average of 12 +/- 2 mosmol/kg in both intact and SAD dogs. Arterial pressure increased 6 +/- 2 mmHg in intact animals and was normalized by subsequent administration of a specific vascular AVP antagonist. Pretreatment with the AVP antagonist did not alter resting arterial pressure but prevented the increase due to the osmotic stimulus. Pretreatment with ganglionic blockade reduced resting arterial pressure (-17 +/- 2 mmHg). Subsequent infusion of hypertonic NaCl elevated arterial pressure (21 +/- 7 mmHg) to a significantly greater level than that observed with the autonomic nervous system intact. In SAD dogs, the osmotic stimulus increased arterial pressure (16 +/- 1 mmHg) to a significantly greater extent than in intact animals. Subsequent administration of AVP antagonist normalized arterial pressure, and pretreatment with the antagonist prevented any pressor response. Pretreatment with ganglionic blockade did not alter the pressor response (15 +/- 2 mmHg) to hypertonic NaCl. Data suggest that the increase in arterial pressure due to an osmotic stimulus is due to AVP release and does not require a functional sympathetic nervous system. The response is normally buffered by arterial baroreflexes, presumably due to sympathetic withdrawal.

Animals↗
PubMed1985

Interactions of vasopressin with the area postrema in arterial baroreflex function in conscious rabbits.

This study compares the effect of arginine-vasopressin with phenylephrine on arterial pressure, heart rate, and renal sympathetic nerve activity in conscious rabbits with and without functional arterial baroreflexes and in rabbits with lesions of the area postrema. In intact rabbits, progressive infusions of arginine-vasopressin result in large decreases in renal sympathetic nerve activity and heart rate for a given increase in blood pressure as compared to progressive infusions of phenylephrine. In sinoaortic-denervated rabbits, the responses of arterial pressure on heart rate and renal sympathetic nerve activity to both arginine-vasopressin and phenylephrine are markedly attenuated, indicating the necessity for afferent baroreceptor activity in this response. This observation indicates that arginine-vasopressin is acting centrally to enhance the baroreflex. A central site of action of circulating vasopressin may be the area postrema, since it is the only circumventricular organ in the hindbrain. Lesioning the region of the area postrema resulted in a normalization of the responses evoked with arginine-vasopressin and phenylephrine. There was no difference in the phenylephrine responses of arterial pressure on renal sympathetic nerve activity or heart rate in area postrema-lesioned animals, compared to control rabbits. Therefore, we conclude that the area postrema or its surrounding tissue is either a site of action of circulating arginine-vasopressin or contains fibers of passage from another site where arginine-vasopressin acts to enhance baroreflex activity.

Animals↗
PubMed1985

Arterial and cardiopulmonary reflexes in the regulation of the neurohumoral drive to the circulation.

The integrative reflex control of the neurohumoral drive to the circulation by unmyelinated vagal afferents and arterial baroreceptor afferents is often complex and depends on a number of factors. These include 1) the initial condition or the existing inhibitory influence exerted by one receptor station, 2) alteration in gain or central response of one reflex as a result of afferent information from the other system, and 3) altered receptor sensitivity as a result of reflex changes in sympathetic outflow. With respect to the cardiopulmonary and arterial baroreflex control of renin release, the accompanying reflex hemodynamic changes may influence the magnitude of the renin response. Finally, recent data suggest that reflex increases in vasopressin by either reflex system may result in an inhibitory influence on sympathetic outflow. Thus, in this latter case, a central interaction results between two reflex responses.

Animals↗
PubMed1984

The role of vasopressin and the sympathetic nervous system in the cardiovascular response to vagal cold block in the conscious dog.

This study examined the role of arginine vasopressin in the pressor response to vagal cold block and evaluated a possible interaction between vasopressin and the sympathetic nervous system during vagal block in conscious dogs with (carotid sinus intact) and without (sinoaortic denervated) functional arterial baroreflexes. In both carotid sinus intact and sinoaortic denervated dogs, elimination of the arginine vasopressin pressor system by the specific vasopressin antagonist d(CH2)5Tyr(Me)AVP did not alter the response to vagal block, as evaluated by changes in arterial pressure. Subsequent removal of the sympathetic nervous system by ganglionic blockade abolished the response to vagal block. When ganglionic blockade was induced in the absence of the vasopressin antagonist, the pressor response to vagal block was reduced by only 60%. Arginine vasopressin antagonist after ganglionic blockade reduced the response to vagal block by an amount equivalent to 45% of the original increase in pressure. The effects of blockade of either vasopressin or the sympathetic nervous system on the pressor response to vagal block were significantly greater when the other system had previously been eliminated. Data suggest that both arginine vasopressin and the sympathetic nervous system contribute to the pressor response to vagal block. One interpretation of these results is that vasopressin also interacts centrally to inhibit sympathetic outflow and thus modulates the hemodynamic manifestation of interruption of vagal afferents.

Animals↗
PubMed1983

Metabolic enzyme response in the pressure-overloaded heart of weanling and adult rats.

Weanling and adult rats were subjected to left ventricular pressure overload induced by abdominal aortic constriction. At 5 days or 5 weeks postsurgery, the left ventricle (LV) was dissected, weighed, and metabolic marker enzyme activities (mumole/g/min) of tissue homogenates were measured. Enzymes representing glycolytic (phosphofructokinase (PFK] and mitochondrial (citrate synthase (CS) and malate dehydrogenase (MDH] metabolisms were evaluated. Five days of pressure overload had detectable, but statistically nonsignificant effects on left ventricles of both weanling and adult rats. Sustained pressure overload (5 weeks) increased LV weight by 52 and 39% in weanling and adult rats, respectively. PFK activity was 24 +/- 1 (mean +/- SE) in control weanlings and was unaltered in any of the other groups. LDH isoenzyme composition was estimated by substrate inhibition (ratio 0.33/10 mM pyruvate). With normal heart development, the LDH ratio increased from 1.89 +/- 0.06 to 2.03 +/- 0.08. Pressure overload had no influence on the adult LDH ratio. Developmental LDH responses were not observed in weanling LV after 5 weeks of aortic constriction (1.74 +/- 0.06). The product of CS activity and LV weight was used to estimate mitochondrial mass in the ventricle. Mitochondria accumulated at a rate of about 5% increase per day over the intervening 5-week period of normal heart growth. Pressure overload for 5 weeks in weanling rats elicited net accumulation of mitochondria at a rate of about 9% increase per day. Mitochondrial accumulation in the adapting adult rat heart amounted to less than 1% increase per day. The results indicate that qualitative and quantitative differences exist between young and adult animals in their heart enzyme adaptive responses to pressure overloading. Divergent metabolic adaptations may contribute to heart functional differences in the enlarged heart of weanlings and adults.

Age Factors↗
PubMed1982

Hemodynamic responses to methoxamine in exercise-conditioned and aorta-constricted rats.

Hemodynamic responses to methoxamine hydrochloride (Vasoxyl) were determined in rats conditioned by a moderate treadmill exercise program and in rats subjected to 5 wk of abdominal aortic constriction. Rats of comparable age served as controls. Initial hemodynamic values for control rats were as follows: left ventricular pressure, 124 +/- 4 Torr and cardiac index, 145 +/- 8 ml . min-1 . kg-1. Although minor variations were noted, initial hemodynamic values for exercise-conditioned rats were within the normal range, and no left ventricular hypertrophy was present. Aorta-constricted rats exhibited a 50% increase in left ventricular weight and significant differences in left ventricular pressure (173 +/- 9 Torr) and cardiac index (117 +/- 10 ml . min-1 . kg-1). Sequentially increasing doses of methoxamine were infused to elevate myocardial preload and afterload. When compared with control rats, exercise-conditioned animals were better able to maintain cardiac index at comparable increases in either mean arterial or left ventricular end-diastolic pressures. In contrast, aorta-constricted rats demonstrated profound reductions in hemodynamic functions in response to methoxamine infusion. Directionally divergent hemodynamic results occur in exercise-conditioned and aorta-constricted animals when subjected to identical cardiovascular stresses.

Animals↗
PubMed1978

Escherichia coli shock in the baboon and the response to adrenocorticosteroid treatment.

Results of recent studies from this laboratory have demonstrated that methylprednisolone sodium succinate increases the survival rate of dogs given LD100 Escherichia coli endotoxin. This study was undertaken to determine the effects of methylprednisolone on the baboon infused with live Escherichia coli organisms. Awake baboons were paired by infusing intravenously comparable doses of Escherichia coli during a five hour period. Baboons given methylprednisolone received bolus injections of 30 milligrams per kilogram at 15 minutes after beginning the infusion of Escherichia coli and two hour infusions of 15 milligrams per kilogram at two hour intervals until death or for a 24 hour period. The mortality was unaltered by methylprednisolone. Six of seven baboons that were dying became progressively hypoglycemic, while hypoinsulinemia occurred in all baboons within six hours and was sustained until death. Systemic hypotension was observed. although pressures were variable. Potassium and lactate concentrations increased, while pH remained relatively constant in most baboons. Serum glutamic-pyruvic transaminase and arginase concentrations rose in most baboons dying with 18 hours. Results of morphologic studies revealed the presence of fibrin thrombi in the liver, kidney and adrenal tissue in most baboons. No significant differences in physiologic, metabolic, hematologic or morphologic parameters were observed between treated and untreated baboons.

Animals↗
PubMed1978

Lymph and intrarenal venous blood as indicators of canine renal cortical function.

Samplings of canine capsular and hilar lymph, and intrarenal venous blood were investigated as in vivo techniques for detecting renal cortical function in control and NH4Cl pretreated anesthetized animals. The glucose concentration of capsular, but not hilar, lymph was indicative of cortical drainage in both groups. When lymph flow was increased by elevating renal venous pressure, capsular lymph glucose concentration reflected cortical function only in the NH4Cl animals. The glucose concentration of intrarenal venous blood indicated cortical drainage in both the control and NH4Cl animals but the cortical function of a high para-aminohippuric acid extraction was only detectable in the NH4Cl group. Conclusions are that sampling of capsular lymph and intrarenal venous blood may prove to be useful techniques for studying certain in vivo cortical functions but the intrarenal venous technique is less sensitive than capsular lymph collection.

Administration, Oral↗
PubMedDate not supplied

Area postrema and sympathetic nervous system effects of vasopressin and angiotensin II.

1. Precise control over the cardiovascular system requires the integration of both neural and humoral signals related to blood volume and blood pressure. Humoral signals interact with neural systems, modulating their control over the efferent mechanisms that ultimately determine the level of pressure and volume. 2. Peptide hormones such as angiotensin (Ang)II and arginine vasopressin (AVP) act through circumventricular organs (CVO) to influence cardiovascular regulation. 3. The area postrema (AP), a CVO in the brainstem, mediates at least some of the central actions of these peptides. Vasopressin appears to act in the AP to cause sympathoinhibition and a shift in baroreflex control of the sympathetic nervous system (SNS) to lower pressures. These effects of AVP and the AP appear to be mediated by alpha2-adrenoceptor and glutamatergic mechanisms in the nucleus tractus solitarius. 4. In contrast to AVP AngII has effects in the AP to blunt baroreflex control of heart rate and cause sympathoexcitation. The effects of chronic AngII to increase activity of the SNS may be due to AP-dependent activation of neurons in the rostral ventrolateral medulla.

Angiotensin II↗