pituitrin and Arterial-Occlusive-Diseases

The genesis of renovascular hypertension follows a continuum from an acute to a chronic phase. Reduction in renal perfusion initiates renin release and angiotensin-mediated systemic vasoconstriction. Aldosterone secretion, sodium and water retention, and expansion of the extracellular volume ensue. Sustained hypertension is further maintained by interacting physiologic mechanisms including increased angiotensin II sensitivity, vasopressin, ouabain-like substance, the sympathetic nervous system, CNS mechanisms, autoregulation, and structural changes.

Topics: Acute Disease; Angiotensin II; Animals; Arterial Occlusive Diseases; Central Nervous System; Chronic Disease; Disease Models, Animal; Dogs; Hemodynamics; Hypertension, Renovascular; Kidney; Ouabain; Perfusion; Rats; Renin-Angiotensin System; Sympathetic Nervous System; Vasoconstriction; Vasopressins

Interventional radiology is defined as a radiologic subspecialty and the services provided are tabulated in this article; those services relevant to internists are described in greater detail. This article is intended as a survey, and the authors encourage the reader to consult the references provided for a more in-depth review.

Topics: Abscess; Angiography; Angioplasty, Balloon; Arterial Occlusive Diseases; Arteriovenous Malformations; Biopsy, Needle; Cholestasis; Drainage; Embolization, Therapeutic; Fibrinolytic Agents; Gastrointestinal Hemorrhage; Hemoptysis; Humans; Neoplasms; Peptic Ulcer; Radiography; Vasopressins

Vasopressin (VP) is a key factor in the development of brain injury in ischemic stroke. However, the regulation of VP secretion in basilar artery occlusion (BAO) remains unclear. To clarify the regulation of VP secretion in BAO and the underlying mechanisms, we performed this study in a rat model of BAO with (BC) or without common carotid artery occlusion (CCAO). The results showed that BAO and BC time-dependently increased neurological scores and that BC also increased water contents in the medulla at 2 h and in the pontine at 8 h. Moreover, plasma VP level increased significantly at BAO-8 h, CCAO and BC-2 h but not at BC-8 h; however, VP expressions increased in the supraoptic nucleus (SON) at BC-8 h. The neurological scores were highly correlated with pontine water contents and plasma VP levels. The number of phosphorylated extracellular signal-regulated protein kinase1/2-positive VP neurons increased significantly in the SON at BC-8 h. Similarly, the number of c-Fos-positive VP neurons increased significantly in the SON at BAO-8 h and BC-8 h. In addition, the length of glial fibrillary acidic protein (GFAP) filaments increased significantly in BC compared to BAO only. Aquaporin 4 (AQP4) puncta around VP neurons increased significantly at BC-8 h relative to BC-2 h, which had negative correlation with plasma VP levels. These findings indicate that BAO facilitates VP secretion and increases VP neuronal activity in the SON. The peripheral VP release is possibly under a negative feedback regulation of central VP neuronal activity through increasing GFAP and AQP4 expression in astrocytic processes.

Topics: Animals; Arterial Occlusive Diseases; Astrocytes; Basilar Artery; Brain; Carotid Artery Diseases; Male; Neuronal Plasticity; Neurons; Rats, Sprague-Dawley; Vasopressins

Extracellular single-unit recording experiments were done in pentobarbital sodium-anesthetized rats to investigate the effects of electrical stimulation of afferent renal nerves (ARN) and renal vein (RVO) or artery (RAO) occlusion on the discharge rate of putative arginine vasopressin (AVP) and oxytocin (Oxy) neurons in the paraventricular nucleus of the hypothalamus (PVH). PVH neurons antidromically activated by electrical stimulation of the neurohypophysis were classified as either AVP or Oxy secreting on the basis of their spontaneous discharge patterns and response to activation of arterial baroreceptors. Ninety-eight putative neurosecretory neurons in the PVH were tested for their response to electrical stimulation of ARN: 44 were classified as putative AVP and 54 as putative Oxy neurons. Of the 44 AVP neurons, 52% were excited, 7% were inhibited, and 41% were nonresponsive to ARN stimulation. Of the 54 Oxy neurons, 43% were excited, 6% inhibited, and 51% were not affected by ARN. An additional 45 neurosecretory neurons (29 AVP and 16 Oxy neurons) were tested for their responses to RVO and/or RAO. RVO inhibited 42% of the putative AVP neurons and 13% of the putative Oxy neurons. On the other hand, RAO excited 33% of the AVP and 9% of the Oxy neurons. No AVP or Oxy neurons were found to be excited by RVO or inhibited by RAO. These data indicate that sensory information originating in renal receptors alters the activity of AVP and Oxy neurons in the PVH and suggest that these renal receptors contribute to the hypothalamic control of AVP and Oxy release into the circulation.

Topics: Afferent Pathways; Animals; Arterial Occlusive Diseases; Cardiovascular System; Constriction, Pathologic; Electric Stimulation; Kidney; Male; Neurons; Neurosecretory Systems; Oxytocin; Paraventricular Hypothalamic Nucleus; Rats; Rats, Wistar; Renal Artery; Renal Veins; Vascular Diseases; Vasopressins

Vascular reactivity, heart rate responses to vasoconstrictor and/or vasodilatator agents and catecholamine and arginine vasopressin turnover were studied in normotensive Wistar Kyoto (WKY), spontaneously hypertensive (SHR), normolipemic Brown Norway (BN) and spontaneously hyperlipemic Yoshida (YOS) anaesthetized rats at 2, 6 and 18 months of age. In this study, we investigated whether ageing and development could affect cardiovascular reactivity to vasoactive substances and catecholamine and arginine vasopressin turnover. No significant changes in the pressor responses to noradrenaline and to carotid sinus baroreceptor stimulation were observed nor were there significant alterations in reflex tachycardia and bradycardia. Arginine vasopressin plasma levels also did not change with ageing and development. On the other hand, the hypotensive responses to isoprenaline decreased in old rats, acetylcholine relaxation effect increased with ageing and development in some rat strains (BN and YOS) and catecholamine plasma levels increased with ageing and development. Our results indicate that during ageing and development, vascular responsiveness to vasoconstrictor and/or vasodilatator agents, as well as amine turnover, may increase, decrease or not change at all depending on the neurotransmission system studied, and on the experimental model and/or animal tested.

Topics: Acetylcholine; Aging; Animals; Arginine; Arterial Occlusive Diseases; Blood Pressure; Carotid Artery Diseases; Catecholamines; Hyperlipidemias; Hypertension; Isoproterenol; Norepinephrine; Rats; Rats, Inbred Strains; Vasomotor System; Vasopressins

Carotid occlusion evoked a pressor response in rats after transection of the spinal cord. Intraventricular pretreatment with 6-hydroxydopamine inhibited the pressor response. The pressor response to occlusion was also diminished by the intraventricular but not by the intravenous injection of guanethidine. Intravenous atropine or mecamylamine, or intraventricular captopril did not affect the pressor response. Thus, it appears that central catecholaminergic mechanisms are involved in the mediation of the pressor response to carotid occlusion.

Topics: Animals; Arterial Occlusive Diseases; Blood Pressure; Brain; Carotid Artery Diseases; Catecholamines; Guanethidine; Male; Rats; Rats, Inbred Strains; Vasopressins

In 18 dogs, intracoronary infusion of vasopressin produced a 40% reduction in coronary flow without significantly affecting systemic hemodynamics. The blood flow reduction occurred in a uniform transmural pattern without evidence of a gradient. The reduction in coronary flow resulted in a decrease in regional contractility as determined by isometric strain gauge arches. The decrease in regional contractility was transiently reversed by bolus injection of adenosine into the perfusion line. This suggests that the reduction of blood flow due to vasopressin was causing ischemia. Evidence for ischemia was also supported by measurements of local vein and tissue lactate production. Despite the apparently ischemic conditions, the vascular bed demonstrated evidence for significant reserve and regulation. Pressure-flow relationships performed under control and during vasopressin infusion demonstrated that the coronary vasculature retained its ability to regulate or defend a given level of coronary flow over a range of coronary perfusion pressures. Vasopressin produced a mild decrease in the peak hyperemic flow after a 15-s coronary occlusion and shortened the duration of reactive hyperemia. These overall findings are compatible with a predominant vasoconstrictor effect on the distal coronary vasculature. A role for a myogenic factor in the control of the coronary circulation is suggested, which is amplified by vasopressin.

Topics: Animals; Arterial Occlusive Diseases; Arteries; Coronary Circulation; Dogs; Female; Hemodynamics; Homeostasis; Hyperemia; Male; Myocardial Contraction; Vasopressins

1 In cats anaesthetized with pentobarbitone sodium or chloralose, the amino acids, gamma-aminobutyric acid (GABA) and glycine, were applied to the ventral surface of the brain through paired Perspex rings placed across the medulla. 2 Applied to a region situated at the transition between medulla and cord, both amino acids greatly attenuated and even abolished the vasopressin release in response to carotid occlusion. Glycine was about 100 times more potent than GABA and effective in a concentration of 0.1 mg/ml. The pressor response to carotid occlusion was not affected. 3 Applied to a region situated 5 to 6 mm more rostrally, the amino acids did not affect vasopressin release but in strong concentrations, greatly attenuated the pressor response to carotid occlusion. 4 The two responses to carotid occlusion, vasopressin release and the pressor response, can thus be influenced independently. 5 It is concluded that the pathways carrying afferent impulses from the baroreceptors in the carotid sinus reach the ventral surface of the brain stem at two regions. At both, synaptic transmission can be blocked by the application of an inhibitory amino acid and thus prevent either the release of vasopressin at the caudal site, or the increase of vasomotor tone at the rostral site.

Topics: Animals; Arterial Occlusive Diseases; Blood Pressure; Brain Stem; Carotid Artery Diseases; Cats; Dose-Response Relationship, Drug; gamma-Aminobutyric Acid; Glycine; Male; Synaptic Transmission; Vasopressins

Topics: Animals; Arterial Occlusive Diseases; Blood Pressure; Coronary Circulation; Coronary Vessels; Dogs; Isoproterenol; Methoxamine; Nitroglycerin; Radiography; Vascular Resistance; Vasomotor System; Vasopressins

Topics: Angiotensin II; Animals; Arterial Occlusive Diseases; Blood Pressure; Carotid Arteries; Carotid Artery Diseases; Catheterization; Depression, Chemical; Dogs; Heart Rate; Heart Ventricles; Hemodynamics; Infusions, Parenteral; Ligation; Lysine; Nitroglycerin; Prostaglandins; Prostaglandins E; Stimulation, Chemical; Transducers; Vagotomy; Vasopressins