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PubMedDate not supplied

Determinants of response of pial arteries to norepinephrine and sympathetic nerve stimulation.

Feline pial arteries larger than 100 mu in diameter constricted in response to cervical sympathetic nerve stimulation suggests or in response to topical application of norepinephrine. Smaller pial arteries were unresponsive to norepinephrine. This unresponsiveness persisted when norepinephrine was dissolved in CSF with high calcium ion concentration, or in CSF with both high calcium ion and zero magnesium ion concentration, or when it was dissolved in the acid fluid used by Wahl et al. and applied by constant infusion or by intermittent application. Comparison of the responses of the larger pial vessels to norepinephrine and to sympathetic nerve stimulation that maximal activation of sympathetic nerves achieves a concentration of released norepinephrine equal to 5.9 x 10(-6) M. The constriction of the larger pial vessels in response to sympathetic nerve stimulation could account for modest reductions in cerebral blood flow.

Animals↗
PubMed2001

Vasopeptidase inhibitors: a new therapeutic concept in cardiovascular disease?

The cardiovascular system is regulated by hemodynamic and neurohumoral mechanisms. These regulatory systems play a key role in modulating cardiac function, vascular tone, and structure. Although neurohumoral systems are essential in vascular homeostasis, they become maladaptive in disease states such as hypertension, coronary disease, and heart failure. The clinical success of ACE inhibitors has led to efforts to block other humoral systems. Neutral endopeptidase (NEP) is an endothelial cell surface zinc metallopeptidase with similar structure and catalytic site. NEP is the major enzymatic pathway for degradation of natriuretic peptides, a secondary enzymatic pathway for degradation of kinins, and adrenomedullin. The natriuretic peptides can be viewed as endogenous inhibitors of the renin angiotensin system. Inhibition of NEP increases levels of atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP) of myocardial cell origin, and C-type natriuretic peptide (CNP) of endothelial cell origin as well as bradykinin and adrenomedullin. By simultaneously inhibiting the renin-angiotensin-aldosterone system and potentiating the natriuretic peptide and kinin systems, vasopeptidase inhibitors reduce vasoconstriction, enhance vasodilation, improve sodium/water balance, and, in turn, decrease peripheral vascular resistance and blood pressure and improve local blood flow. Within the blood vessel wall, this leads to a reduction of vasoconstrictor and proliferative mediators such as angiotensin II and increased local levels of bradykinin (and, in turn, nitric oxide) and natriuretic peptides. Preliminary clinical experiences with vasopeptidase inhibitors are encouraging. Thus, the combined inhibition of ACE and neutral endopeptidase is a new and promising approach to treat patients with hypertension, atherosclerosis, or heart failure.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1984

Systemic circulatory adjustments to acute hypoxia and reoxygenation in unanesthetized sheep. Role of renin, angiotensin II, and catecholamine interactions.

The hemodynamic consequences of the hypoxic inhibition of angiotensin-converting enzyme activity were studied in chronically instrumented unanesthetized sheep (n = 8) breathing a hypoxic gas mixture for 60 min (PaO2 = 31 mm Hg) followed by reoxygenation with room air. Changes in cardiac output, vascular pressures, blood flow distribution, arterial pH, PaCO2, PaO2, and arterial levels of plasma renin activity, angiotensin II, bradykinin, and catecholamines were measured at selected time points. Seven additional sheep underwent the same protocol but received saralasin, an angiotensin II receptor blocker beginning at 55 min of hypoxia and extending into the reoxygenation period. During hypoxia, both groups developed identical hemodynamic patterns including a rise in cardiac output (25%), blood pressure (15%), and preferential blood flow distribution to the heart, brain, adrenals, diaphragm, and skeletal muscle, as well as a decrease in the fraction of cardiac output to the kidneys and most of the gut. This was associated with a decrease in angiotensin II concentrations (from 35 to 17 pg/ml) in spite of a doubling in plasma renin activity and catecholamines. Bradykinin levels did not change. Upon reoxygenation, bolus production of angiotensin II (from 17 to 1,819 pg/ml) occurred in spite of a constant level of plasma renin activity. Concurrently, different hemodynamic patterns between control and saralasin groups emerged upon reoxygenation, including an elevation from base line in blood pressure and systemic vascular resistance in the control group. Cardiac work (heart-rate systolic pressure product) in the control group remained elevated upon reoxygenation while coronary blood flow returned to base-line values. Saralasin reduced cardiac work upon reoxygenation and restored the match between coronary blood flow and work. We conclude that plasma renin activity and oxygen tension together govern angiotensin II levels for an optimal level of systemic vasomotor tone during hypoxia. However, upon reoxygenation, bolus production of angiotensin II may result in pathophysiologic circulatory patterns, such as impairment in oxygen delivery to the myocardium proportional to persistently elevated cardiac work in the immediate postresuscitation period.

Angiotensin II↗
PubMed1994

Inhibition of nitric oxide synthesis improves the vasoconstrictive effect of noradrenaline in sepsis.

BACKGROUND: Septic shock is characterized by systemic vasodilation and an impaired reactivity to vasoconstrictor agents. It has been suggested that an excessive release of nitric oxide has a role in this hemodynamic derangement. OBJECTIVE: To investigate whether inhibition of nitric oxide synthesis by the administration of N omega-nitro-L-arginine (LNNA), improves the vasoconstrictor effects of catecholamines in sepsis. MATERIAL AND METHODS: Mechanically ventilated and pentobarbital-anesthetized sheep received either no treatment (n = 6) or LNNA (100 mg/kg IV bolus, n = 4). Other sheep (septic group) received live Escherichia coli (E coli) (1,5* 10(9) micro-organisms/kg over 30 min) followed 1 hour later by either no treatment (n = 5) or LNNA (100 mg/kg IV bolus, n = 7). After those interventions, all sheep were given noradrenaline in a continuous IV infusion at three different doses (0.5, 1.5, and 4.5 micrograms, kg-1, min-1). Cardiovascular parameters were recorded at maximal blood pressure response achieved with each dose. RESULTS: The administration of live E coli to the septic group resulted in systemic hypotension, high cardiac output, and hyperlactatemia. The LNNA caused a significant systemic and pulmonary vasoconstriction in both septic and nonseptic sheep. In nonseptic sheep, noradrenaline induced a significant increase in systemic vascular resistance (from 2,973 +/- 637 to 4,561 +/- 1,287 dyn/s/cm-5/m-2), whereas the increase caused in those that received LNNA was nonsignificant (5,562 +/- 3,489 to 6,693 +/- 2,871 dyn, s, cm-5, m-2). Septic sheep showed a nonsignificant vasoconstriction during the infusion of noradrenaline (from 1,438 +/- 1,132 to 2,244 +/- 1,391 dyn/s/cm-5/m-2). However, treatment with LNNA markedly improved the vasoconstrictor effect of noradrenaline (from 2,804 +/- 2,317 to 4,894 +/- 3,435 dyn/s/cm-5/m-2). The dose-response curve of systemic vascular resistance in these LNNA-pretreated septic sheep became very similar to the corresponding curve obtained in nonseptic animals. CONCLUSIONS: Inhibition of nitric oxide synthesis by the administration of LNNA significantly improves the vasoconstrictor effect of noradrenaline in septic sheep, allowing an increase in systemic vasomotor tone similar to that observed in nonseptic sheep. It is concluded that increased synthesis of nitric oxide contributes to the depressed vascular reactivity to vasoconstrictor agents characteristic of sepsis.

Animals↗
PubMed1977

Influence of local insults on sympathetic vasoconstrictor control in feline dental pulp.

The present investigation was undertaken to ascertain whether local insults can affect the sympathetic vasoconstrictor regulation of pulpal blood flow. The rate of disapperance (k-value) of iodide from dentinal cavities was measured in anaesthetized cats. Changes in k-value reflected changes in blood flow. It has previously been shown that stimulation of sympathetic vasoconstrictor nerve fibres generally causes a clearcut decrease in the k-value. Deep cavity preparation was found to inhibit the vasoconstrictor response in a few cases in experiments on mature cats. Heating or cooling the tooth during cavity preparation induced a more frequent inhibition, which proved to be reversible within a few hours. Compound 48/80 applied locally to the cavity was also found to induce inhibition of the vasoconstrictor effect, but in this case no sign of reversibility was observed. Chronic insults were produced by exposing the cavity to oral microorganisms during 1-4 weeks before the experimental procedure. In this case, the sympathetic vasoconstrictor response was not inhibited. A histological study was performed to examine the pulp tissue after cavity preparation and the application of insults. It was found that cavity preparation and acute insults caused little or no disturbance, while chronic insults resulted in severe damage to the pulpal tissue.

Administration, Topical↗
PubMed1988

Effects of the alpha-adrenoceptor antagonists phentolamine, phenoxybenzamine, and idazoxan on sympathetic blood flow control in the periodontal ligament of the cat.

Blood flow changes in the periodontal ligament (PDL) were measured indirectly by monitoring the local clearance of 125I- during electric sympathetic nerve stimulation or close intra-arterial infusions of either noradrenaline (NA) or adrenaline (ADR) before and after administration of phentolamine (PA), phenoxybenzamine (PBZ), or Idazoxan (RX). At the doses used in the present study, PA was the only antagonist that significantly reduced the blood flow decrease seen on activation of sympathetic fibers, although PBZ also reduced this response. Idazoxan, however, did not induce the consistent effect on blood flow decreases seen on sympathetic activation. All three alpha-adrenoceptor antagonists almost abolished the effects of exogenously administered NA and ADR. The results suggest the presence of functional post-junctional adrenoceptors of both the alpha 1 and alpha 2 subtypes in the sympathetic regulation of blood flow in the PDL of the cat. A component of the response elicited by electrical sympathetic stimulation appeared to be resistant to alpha-adrenoceptor blockade. Administration of guanethidine (which inhibits further release of NA and neuropeptide Y) after PA abolished this residual sympathetic response.

Adrenergic alpha-Antagonists↗
PubMedDate not supplied

Plethysmography as an objective method of audiometry.

In 37 subjects with normal hearing acuity and normal cardiovascular system, vasomotor reactions to sounds of 1024, 2048, and 4096 Hz frequency and 0, 10, 20, 60 and 80 dB intensity above the hearing threshold determined were studied subjectively. Pure sounds evoked in all persons plethysmographic reactions not subject to extinction under the conditions of audiometric investigation.

Acoustic Stimulation↗
PubMedDate not supplied

Sympathetic nerve pathways to the nasal vasculature of the cat.

The sympathetic nerve pathways to the nasal vasculature were examined in 8 cats by recoding the effects of section of the orbital nerves on vasoconstriction produced by cervical sympathetic nerve stimulation. No sympathetic fibres were found in the sphenopalatine and infraorbital nerves. The majority were conveyed by either the Vidian or ethmoidal nerves, the remaining fibres are believed to reach the nasal cavity by the periarterial plexus.

Animals↗