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T Unger

Publications and source records attributed to T Unger.

401 records · Page 23Linked to original sources
PubMedDate not supplied

Angiotensin as neuromodulator/neurotransmitter in central control of body fluid and electrolyte homeostasis.

Stimulation of central angiotensin receptors promotes, among others, drinking behaviour, stimulation of natriuresis and increased release of vasopressin. Angiotensin (ANG II)-containing pathways in the lamina terminalis and the hypothalamic paraventricular (PVN) and supraoptic (SON) nuclei, brain areas involved in the regulation of body fluid homeostasis, have been described. All these areas express predominantly AT1 receptors. The drinking response and the vasopressin release to centrally administered ANG II are mediated by AT1 receptors, while AT2 receptors exert inhibitory effects. Evidence for the involvement of the catecholaminergic and angiotensinergic pathways in the PVN and SON in mediating the ANG II-induced release of vasopressin is presented. ANG II is released in the PVN upon local osmotic stimulation and water deprivation. Finally, we present evidence that activation of central angiotensinergic receptors, water deprivation, or hypertonicity induce transcription of immediate-early genes and expression of the respective proteins in the lamina terminalis and in the PVN and SON. The summarized data implicate ANG II as a neuromodulator/neurotransmitter in central control of body fluid and electrolyte homeostasis.

Angiotensin II↗
PubMedDate not supplied

Vasopressin: mechanism of central cardiovascular action in conscious rats.

Arginine vasopressin (AVP) and AVP binding sites have been localized in brain areas involved in cardiovascular control. To elucidate the mechanisms by which brain AVP may participate in central blood pressure regulation, we investigated the effects of central AVP receptor stimulation on mean arterial pressure (MAP), heart rate (HR), efferent splanchnic nerve (SpNA), and renal nerve activity (RNA) in conscious chronically instrumented rats. Intracerebroventricular (i.c.v.) injections of AVP (1-100 ng) produced dose-dependent increases in MAP together with marked increases in HR, SpNA, and RNA. The pressor responses were inhibited by peripheral alpha-adrenoceptor blockade with i.v. phentolamine. In contrast, the pressor responses to either i.v. or intracarotid injections of AVP were accompanied by baroreceptor reflex (BRR)-mediated decreases in HR and SpNA. Central (i.c.v.) pretreatment with d(CH2)5AVP, a V1-AVP receptor antagonist, completely abolished the responses to i.c.v. but not to i.v. AVP. The same antagonist had no effect on the responses to i.c.v. angiotensin II. Our results demonstrate that: (a) central AVP overrides the BRR by sympathetic stimulation, whereas blood-borne AVP activates the BRR; (b) specific AVP receptors in the brain probably of the V1-subtype are involved in the central pressor responses to AVP; (c) the central pressor actions of AVP are transmitted to the periphery by stimulation of the sympathetic nervous system. We conclude that brain AVP may contribute to central cardiovascular control by modulating the sympathetic outflow to the periphery.

Angiotensin II↗
PubMedDate not supplied

A new formalin test allowing simultaneous evaluation of cardiovascular and nociceptive responses.

The formalin test for nociception, predominantly used with rodents, is characterized by continuous pain due to tissue injury induced by formalin. In addition to the pain generated by formalin itself, the classical formalin test for nociception comprises a number of additional strong stressful events such as restraint and injury caused by needle insertion. These events have hampered its use as a model of stress employing continuous pain as a stress stimulus. We describe here a new, simple method of a subcutaneous application of formalin in conscious rats without restraint and needle insertion. Formalin or physiological saline (controls) was injected subcutaneously through a chronically implanted catheter in the region of the lower leg. In most animals, the cardiovascular and behavioural responses to subcutaneously injected formalin were biphasic. The early phase was quantitatively characterized. Formalin (2.5%, 50 microL) induced a marked increase in mean arterial pressure and heart rate. Maximal increases occurred during the first 3 min after formalin injection and were followed by a gradual decline of both cardiovascular parameters to levels higher than the preinjection baseline. Subcutaneous saline injection did not induce any changes in mean arterial pressure and heart rate. The behavioural response to formalin featured intensive licking and biting of the injection site. The behavioural response to subcutaneous saline did not differ from the spontaneous behavioural activity recorded in noninjected rats. Subcutaneously injected formalin induced an immediate increase in plasma corticotrophin (ACTH), corticosterone, noradrenaline, and adrenaline levels, and all hormones remained increased during the whole observation period (60 min). Adrenaline and noradrenaline levels in plasma were slightly, but significantly, elevated during the initial 5 min after subcutaneous saline application but returned to basal values after 15 min. The magnitude of the hormonal responses characterizes the described formalin test as a moderate stress stimulus. The complex response pattern to formalin injected through the subcutaneous catheter is brought about exclusively by pain generated by formalin-induced tissue injury. The described technique of subcutaneous formalin injection represents a new tool to study mechanisms activating brain neuronal circuits that generate the cardiovascular, endocrine, and behavioural responses of the reaction to pain.

Animals↗