@article{MTMT:34482135,
	title = {NO Deficiency Compromises Inter- and Intrahemispheric Blood Flow Adaptation to Unilateral Carotid Artery Occlusion},
	url = {https://m2.mtmt.hu/api/publication/34482135},
	author = {Hricisák, László and Pál, Éva and Nagy, Dorina and Delank, Max and Polycarpou, Andreas and Fülöp, Ágnes and Sándor, Péter and Sótonyi, Péter and Ungvári, Zoltán István and Benyó, Zoltán},
	doi = {10.3390/ijms25020697},
	journal-iso = {INT J MOL SCI},
	journal = {INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES},
	volume = {25},
	unique-id = {34482135},
	issn = {1661-6596},
	abstract = {Carotid artery stenosis (CAS) affects approximately 5–7.5% of older adults and is recognized as a significant risk factor for vascular cognitive impairment (VCI). The impact of CAS on cerebral blood flow (CBF) within the ipsilateral hemisphere relies on the adaptive capabilities of the cerebral microcirculation. In this study, we aimed to test the hypothesis that the impaired availability of nitric oxide (NO) compromises CBF homeostasis after unilateral carotid artery occlusion (CAO). To investigate this, three mouse models exhibiting compromised production of NO were tested: NOS1 knockout, NOS1/3 double knockout, and mice treated with the NO synthesis inhibitor L-NAME. Regional CBF changes following CAO were evaluated using laser-speckle contrast imaging (LSCI). Our findings demonstrated that NOS1 knockout, NOS1/3 double knockout, and L-NAME-treated mice exhibited impaired CBF adaptation to CAO. Furthermore, genetic deficiency of one or two NO synthase isoforms increased the tortuosity of pial collaterals connecting the frontoparietal and temporal regions. In conclusion, our study highlights the significant contribution of NO production to the functional adaptation of cerebrocortical microcirculation to unilateral CAO. We propose that impaired bioavailability of NO contributes to the impaired CBF homeostasis by altering inter- and intrahemispheric blood flow redistribution after unilateral disruption of carotid artery flow.},
	year = {2024},
	eissn = {1422-0067},
	orcid-numbers = {Hricisák, László/0000-0001-8320-2166; Pál, Éva/0000-0003-1793-1912; Nagy, Dorina/0000-0003-2067-753X; Fülöp, Ágnes/0000-0001-8132-2084; Sándor, Péter/0000-0002-1257-8235; Sótonyi, Péter/0000-0002-2216-4298; Ungvári, Zoltán István/0000-0002-6035-6039; Benyó, Zoltán/0000-0001-6015-0359}
}

@article{MTMT:31365424,
	title = {Ablation of Vitamin D Signaling Compromises Cerebrovascular Adaptation to Carotid Artery Occlusion in Mice},
	url = {https://m2.mtmt.hu/api/publication/31365424},
	author = {Pál, Éva and Hricisák, László and Lékai, Á. and Nagy, Dorina and Fülöp, Ágnes and Erben, R.G. and Várbíró, Szabolcs and Sándor, Péter and Benyó, Zoltán},
	doi = {10.3390/cells9061457},
	journal-iso = {CELLS-BASEL},
	journal = {CELLS},
	volume = {9},
	unique-id = {31365424},
	year = {2020},
	eissn = {2073-4409},
	orcid-numbers = {Pál, Éva/0000-0003-1793-1912; Hricisák, László/0000-0001-8320-2166; Nagy, Dorina/0000-0003-2067-753X; Fülöp, Ágnes/0000-0001-8132-2084; Várbíró, Szabolcs/0000-0002-7109-6906; Sándor, Péter/0000-0002-1257-8235; Benyó, Zoltán/0000-0001-6015-0359}
}

@misc{MTMT:30519748,
	title = {NOS izoenzimek szerepe az egér agykérgi váráramlásának szabályozásában},
	url = {https://m2.mtmt.hu/api/publication/30519748},
	author = {Hricisák, László and Simoes, Dobrydnio L and Jabronka, N and Portörő-Gál, P and Janovicz, Anna and Polycarpou, A and Ruisanchez, Éva and Sándor, Péter and Benyó, Zoltán},
	unique-id = {30519748},
	year = {2018},
	orcid-numbers = {Hricisák, László/0000-0001-8320-2166; Janovicz, Anna/0000-0003-3383-5576; Ruisanchez, Éva/0000-0001-7779-226X; Sándor, Péter/0000-0002-1257-8235; Benyó, Zoltán/0000-0001-6015-0359}
}

@misc{MTMT:3243370,
	title = {A NITROGÉN-MONOXID SZEREPE A REGIONÁLIS AGYKÉRGI VÉRÁRAMLÁS SZABÁLYOZÁSÁBAN FÉLOLDALI ARTERIA CAROTIS ELZÁRÁS UTÁN},
	url = {https://m2.mtmt.hu/api/publication/3243370},
	author = {Hricisák, László and Polycarpou, A and Iring, András and Safar, D and Ruisanchez, Éva and Horváth, Béla András and Sándor, Péter and Benyó, Zoltán},
	unique-id = {3243370},
	year = {2017},
	orcid-numbers = {Hricisák, László/0000-0001-8320-2166; Iring, András/0000-0002-3087-4337; Ruisanchez, Éva/0000-0001-7779-226X; Sándor, Péter/0000-0002-1257-8235; Benyó, Zoltán/0000-0001-6015-0359}
}

@article{MTMT:3100748,
	title = {Adaptation of the Cerebrocortical Circulation to Carotid Artery Occlusion Involves Blood Flow Redistribution between Cortical Regions and is Independent of eNOS},
	url = {https://m2.mtmt.hu/api/publication/3100748},
	author = {Polycarpou, A and Hricisák, László and Iring, András and Safar, D and Ruisanchez, Éva and Horváth, Béla András and Sándor, Péter and Benyó, Zoltán},
	doi = {10.1152/ajpheart.00197.2016},
	journal-iso = {AM J PHYSIOL HEART C},
	journal = {AMERICAN JOURNAL OF PHYSIOLOGY: HEART AND CIRCULATORY PHYSIOLOGY},
	volume = {311},
	unique-id = {3100748},
	issn = {0363-6135},
	abstract = {Cerebral circulation is secured by feed-forward and feed-back control pathways to maintain and eventually reestablish the optimal oxygen and nutrient supply of neurons in case of disturbances of the cardiovascular system. Using the high temporal and spatial resolution of laser-speckle imaging we aimed to analyze the pattern of cerebrocortical blood flow (CoBF) changes after unilateral (left) carotid artery occlusion (CAO) in anesthetized mice in order to evaluate the contribution of macrovascular (Willis circle) vs. pial collateral vessels as well as that of endothelial nitric oxide synthase (eNOS) to the cerebrovascular adaptation to CAO. In wild-type mice CoBF reduction in the left temporal cortex started immediately after CAO, reaching its maximum (-26%) at 5-10 s. Thereafter, CoBF recovered close to the pre-occlusion level within 30 s indicating the activation of feed-back pathway(s). Interestingly, the frontoparietal cerebrocortical regions also showed CoBF reduction in the left (-17-19%) but not in the right hemisphere, although these brain areas receive their blood supply from the common azygos anterior cerebral artery in mice. In eNOS-deficient animals the acute CoBF reduction after CAO was unaltered, and the recovery was even accelerated as compared to controls. These results indicate that (i) the Willis circle alone is not sufficient to provide an immediate compensation for the loss of one carotid artery, (ii) pial collaterals attenuate the ischemia of the temporal cortex ipsilateral to CAO at the expense of the blood supply of the frontoparietal region, and (iii) eNOS, surprisingly, does not play an important role in this CoBF redistribution.},
	year = {2016},
	eissn = {1522-1539},
	pages = {H972-H980},
	orcid-numbers = {Hricisák, László/0000-0001-8320-2166; Iring, András/0000-0002-3087-4337; Ruisanchez, Éva/0000-0001-7779-226X; Sándor, Péter/0000-0002-1257-8235; Benyó, Zoltán/0000-0001-6015-0359}
}

@book{MTMT:3013894,
	title = {Az agyi vérkeringés élettani alapjai: önszabályozó mechanizmusok},
	url = {https://m2.mtmt.hu/api/publication/3013894},
	isbn = {9789633313756},
	author = {Sándor, Péter and Benyó, Zoltán},
	publisher = {Semmelweis Kiadó és Multimédia Stúdió Kft.},
	unique-id = {3013894},
	year = {2016},
	orcid-numbers = {Sándor, Péter/0000-0002-1257-8235; Benyó, Zoltán/0000-0001-6015-0359}
}

@article{MTMT:3011598,
	title = {Endocannabinoids in Cerebrovascular Regulation},
	url = {https://m2.mtmt.hu/api/publication/3011598},
	author = {Benyó, Zoltán and Ruisanchez, Éva and Leszl-Ishiguro, Mirjam and Sándor, Péter and Pacher, Pál},
	doi = {10.1152/ajpheart.00571.2015},
	journal-iso = {AM J PHYSIOL HEART C},
	journal = {AMERICAN JOURNAL OF PHYSIOLOGY: HEART AND CIRCULATORY PHYSIOLOGY},
	volume = {310},
	unique-id = {3011598},
	issn = {0363-6135},
	abstract = {The cerebral blood flow (CBF) is tightly regulated by myogenic, endothelial, metabolic and neural mechanisms under physiological conditions, and a large body of recent evidence indicates that inflammatory pathways have a major influence on the cerebral blood perfusion in certain CNS disorders, like hemorrhagic and ischemic stroke, traumatic brain injury and vascular dementia. All major cell types involved in cerebrovascular control pathways (i.e. smooth muscle, endothelium, neurons, astrocytes, pericytes, microglia and leukocytes) are capable of synthesizing endocannabinoids and/or express some or several of their target proteins (i.e. the cannabinoid 1 and 2 receptors (CB1 and CB2) and the TRPV1 ion channel). Therefore, the endocannabinoid system may importantly modulate the regulation of cerebral circulation under physiological and pathophysiological conditions in a very complex manner. Experimental data accumulated since the late 1990s indicate that the direct effect of cannabinoids on cerebral vessels is vasodilation mediated, at least in part, by CB1 receptors. Cannabinoid-induced cerebrovascular relaxation involves both a direct inhibition of smooth muscle contractility and a release of vasodilator mediator(s) from the endothelium. However, under stress conditions (e.g. in conscious restrained animals or during hypoxia and hypercapnia) cannabinoid receptor activation was shown to induce a reduction of the CBF, probably via inhibition of the electrical and/or metabolic activity of neurons. Finally, in certain cerebrovascular pathologies (e.g. subarachnoid hemorrhage as well as traumatic and ischemic brain injury) activation of CB2 (and probably yet unidentified non-CB1/non-CB2) receptors appear to improve the blood perfusion of the brain via attenuating vascular inflammation.},
	year = {2016},
	eissn = {1522-1539},
	pages = {H785-H801},
	orcid-numbers = {Benyó, Zoltán/0000-0001-6015-0359; Ruisanchez, Éva/0000-0001-7779-226X; Sándor, Péter/0000-0002-1257-8235; Pacher, Pál/0000-0001-7036-8108}
}

@misc{MTMT:30792746,
	title = {Endocannabinoidok szerepe az agyi vérkeringés szabályozásában},
	url = {https://m2.mtmt.hu/api/publication/30792746},
	author = {Benyó, Zoltán and Ruisanchez, Éva and Iring, András and Leszl-Ishiguro, Miriam and Sándor, Péter and Pacher, Pál},
	unique-id = {30792746},
	year = {2015},
	orcid-numbers = {Benyó, Zoltán/0000-0001-6015-0359; Ruisanchez, Éva/0000-0001-7779-226X; Iring, András/0000-0002-3087-4337; Sándor, Péter/0000-0002-1257-8235; Pacher, Pál/0000-0001-7036-8108}
}

@inbook{MTMT:3063231,
	title = {Az agyi vérellátás szabályozása. A mikrokeringés regulációjának fő tényezői.},
	url = {https://m2.mtmt.hu/api/publication/3063231},
	author = {Sándor, Péter},
	booktitle = {Vascularis neurológia},
	unique-id = {3063231},
	year = {2015},
	pages = {15-30},
	orcid-numbers = {Sándor, Péter/0000-0002-1257-8235}
}

@article{MTMT:2181946,
	title = {Role of endocannabinoids and cannabinoid-1 receptors in cerebrocortical blood flow regulation},
	url = {https://m2.mtmt.hu/api/publication/2181946},
	author = {Iring, András and Ruisanchez, Éva and Leszl-Ishiguro, Mirjam and Horváth, Béla András and Benkő, Rita and Lacza, Zsombor and Járai, Zoltán and Sándor, Péter and Di Marzo, V and Pacher, Pál and Benyó, Zoltán},
	doi = {10.1371/journal.pone.0053390},
	journal-iso = {PLOS ONE},
	journal = {PLOS ONE},
	volume = {8},
	unique-id = {2181946},
	issn = {1932-6203},
	abstract = {BACKGROUND: Endocannabinoids are among the most intensively studied lipid mediators of cardiovascular functions. In the present study the effects of decreased and increased activity of the endocannabinoid system (achieved by cannabinoid-1 (CB1) receptor blockade and inhibition of cannabinoid reuptake, respectively) on the systemic and cerebral circulation were analyzed under steady-state physiological conditions and during hypoxia and hypercapnia (H/H). METHODOLOGY/PRINCIPAL FINDINGS: In anesthetized spontaneously ventilating rats the CB1-receptor antagonist/inverse agonist AM-251 (10 mg/kg, i.v.) failed to influence blood pressure (BP), cerebrocortical blood flow (CoBF, measured by laser-Doppler flowmetry) or arterial blood gas levels. In contrast, the putative cannabinoid reuptake inhibitor AM-404 (10 mg/kg, i.v.) induced triphasic responses, some of which could be blocked by AM-251. Hypertension during phase I was resistant to AM-251, whereas the concomitant CoBF-increase was attenuated. In contrast, hypotension during phase III was sensitive to AM-251, whereas the concomitant CoBF-decrease was not. Therefore, CoBF autoregulation appeared to shift towards higher BP levels after CB1-blockade. During phase II H/H developed due to respiratory depression, which could be inhibited by AM-251. Interestingly, however, the concomitant rise in CoBF remained unchanged after AM-251, indicating that CB1-blockade potentially enhanced the reactivity of the CoBF to H/H. In accordance with this hypothesis, AM-251 induced a significant enhancement of the CoBF responses during controlled stepwise H/H. CONCLUSION/SIGNIFICANCE: Under resting physiological conditions CB1-receptor mediated mechanisms appear to have limited influence on systemic or cerebral circulation. Enhancement of endocannabinoid levels, however, induces transient CB1-independent hypertension and sustained CB1-mediated hypotension. Furthermore, enhanced endocannabinoid activity results in respiratory depression in a CB1-dependent manner. Finally, our data indicate for the first time the involvement of the endocannabinoid system and CB1-receptors in the regulation of the cerebral circulation during H/H and also raise the possibility of their contribution to the autoregulation of CoBF.},
	year = {2013},
	eissn = {1932-6203},
	orcid-numbers = {Iring, András/0000-0002-3087-4337; Ruisanchez, Éva/0000-0001-7779-226X; Benkő, Rita/0000-0001-7740-9128; Sándor, Péter/0000-0002-1257-8235; Pacher, Pál/0000-0001-7036-8108; Benyó, Zoltán/0000-0001-6015-0359}
}