Actions of angiotensin and lisinopril on thalamic somatosensory neurons in normotensive, non-transgenic and hypertensive, transgenic rats.
OBJECTIVE
To investigate the effects of angiotensin II on discharge rates of somatosensory thalamic neurons and whether these effects are altered in hypertensive transgenic rats [TGR(mREN-2)27] and by long-term treatment with the angiotensin converting enzyme inhibitor lisinopril.


METHODS
Three strains of rats anesthetized with urethane were used (normotensive Wistar and Sprague-Dawley rats (SDR), and [TGR(mREN-2)27]). In addition, the effects of lisinopril treatment on SDR and transgenic animals were tested. The neuronal discharge frequency and the pattern were recorded extracellularly, and their behaviors in response to angiotensin and angiotensin antagonists administered iontophoretically were analyzed.


RESULTS
Angiotensin-sensitive neurons located in the ventral posteromedial and ventral posterolateral thalamic nuclei, and in the zona incerta were excited mainly by angiotensin II. The increase in the firing rates induced by administration of angiotensin II often coincided with an increase in the number of bursts of discharges. Effects induced by angiotensin II could be blocked by administration of specific antagonists (losartan, PD 123319). Long-term treatment with lisinopril reduced the neuronal responsiveness to angiotensin II in SDR significantly in comparison with that of untreated SDR controls. Lisinopril-treated SDR had a significantly lower responsiveness to angiotensin II than did hypertensive transgenic rats that had been treated with lisinopril.


CONCLUSIONS
The results show for the first time that administration of angiotensin II induced changes in discharge rates of somatosensory neurons, and that long-term administration of lisinopril caused a significant difference between the neuronal responsiveness to angiotensin of normotensive SDR and that of hypertensive transgenic rats.
Albrecht
D
D
Institute of Physiology, Faculty of Medicine (Charité), Humboldt University, Berlin, Germany.
Henklein
P
P
Ganten
D
D
D000804:Angiotensin II / Q000494:pharmacology*; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology*; D000818:Animals; D030801:Animals, Genetically Modified; D000959:Antihypertensive Agents / Q000494:pharmacology; D004195:Disease Models, Animal; D004569:Electroencephalography; D006973:Hypertension / Q000188:drug therapy / Q000503:physiopathology*; D007093:Imidazoles / Q000494:pharmacology; D017706:Lisinopril / Q000494:pharmacology*; D019808:Losartan / Q000494:pharmacology; D008297:Male; D009475:Neurons, Afferent / Q000187:drug effects* / Q000502:physiology; D011725:Pyridines / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D017208:Rats, Wistar; D013788:Thalamus / Q000187:drug effects* / Q000502:physiology; D014662:Vasoconstrictor Agents / Q000494:pharmacology*
D000806:Angiotensin-Converting Enzyme Inhibitors; D000959:Antihypertensive Agents; D007093:Imidazoles; D011725:Pyridines; D014662:Vasoconstrictor Agents; D000804:Angiotensin II; C073402:PD 123319; D017706:Lisinopril; D019808:Losartan