Carlos M. Ferrario

ORCID: 0000-0003-0792-6239
Publications
Citations
Views
---
Saved
---
About
Contact & Profiles
Research Areas
  • Renin-Angiotensin System Studies
  • Hormonal Regulation and Hypertension
  • Receptor Mechanisms and Signaling
  • Blood Pressure and Hypertension Studies
  • Neuropeptides and Animal Physiology
  • Apelin-related biomedical research
  • Coagulation, Bradykinin, Polyphosphates, and Angioedema
  • Neuroendocrine regulation and behavior
  • Heart Rate Variability and Autonomic Control
  • Neuroscience of respiration and sleep
  • Cardiovascular, Neuropeptides, and Oxidative Stress Research
  • Mast cells and histamine
  • Estrogen and related hormone effects
  • Nitric Oxide and Endothelin Effects
  • Birth, Development, and Health
  • Adipose Tissue and Metabolism
  • Sodium Intake and Health
  • Hemodynamic Monitoring and Therapy
  • Electrolyte and hormonal disorders
  • Protein Hydrolysis and Bioactive Peptides
  • Stress Responses and Cortisol
  • Lipoproteins and Cardiovascular Health
  • Heart Failure Treatment and Management
  • Eicosanoids and Hypertension Pharmacology
  • Pregnancy and preeclampsia studies

Atrium Health Wake Forest Baptist
1998-2024

Wake Forest University
2015-2024

Ferrari (Italy)
1983-2019

University of Alabama at Birmingham
2017-2018

Pulmonary and Allergy Associates
2017

Ochsner Medical Center
2017

University of Puerto Rico System
2017

McGill University
2014

Jewish General Hospital
2014

Birmingham VA Medical Center
2013

Background— Angiotensin-converting enzyme 2 (ACE2) has emerged as a novel regulator of cardiac function and arterial pressure by converting angiotensin II (Ang II) into the vasodilator antitrophic heptapeptide, angiotensin-(1–7) [Ang-(1–7)]. As only known human homolog ACE, demonstration that ACE2 is insensitive to blockade ACE inhibitors prompted us define effect inhibition on gene. Methods Results— Blood pressure, rate, plasma tissue levels Ang Ang-(1–7), together with ACE2, neprilysin,...

10.1161/circulationaha.104.510461 article EN Circulation 2005-05-17

We investigated in Lewis normotensive rats the effect of coronary artery ligation on expression cardiac angiotensin-converting enzymes (ACE and ACE 2) angiotensin II type-1 receptors (AT1a-R) 28 days after myocardial infarction. Losartan, olmesartan, or vehicle (isotonic saline) was administered via osmotic minipumps for sham operation. Coronary caused left ventricular dysfunction hypertrophy. These changes were associated with increased plasma concentrations I, II, angiotensin-(1-7), serum...

10.1161/01.hyp.0000124667.34652.1a article EN Hypertension 2004-03-09

Abstract Angiotensin-(1-7) [Ang-(1-7)] was recently recognized to have novel biological functions that are distinct from those of Ang II. In these studies, we determined the vasoactive effects Ang-(1-7) together with endothelium-dependent mediator(s) responses in canine coronary arteries. Isometric tension measured intact artery rings suspended organ chambers perfused 95% O 2 /5% CO at 37°C. caused significant concentration-dependent vascular relaxation (2.73±0.58 μmol/L, EC 50 )...

10.1161/01.hyp.27.3.523 article EN Hypertension 1996-03-01

Angiotensin (Ang)-converting enzyme 2 (ACE2) cleaves Ang II to form Ang-(1-7). Here we examined whether soluble human recombinant ACE2 (rACE2) can efficiently lower and increase Ang-(1-7) rACE2 prevent hypertension caused by infusion as a result of systemic versus local mechanisms activity amplification. was infused via osmotic minipumps for 3 days in conscious mice or acutely anesthetized mice. dose-dependent serum but had no effect on kidney cardiac activity. After (40 pmol/min), (1 mg/kg...

10.1161/hypertensionaha.109.138420 article EN Hypertension 2009-12-01

Peptide hormones such as ANG II and endothelin contribute to cardiac remodeling after myocardial infarction by stimulating myocyte hypertrophy myofibroblast proliferation. In contrast, angiotensin-(1-7) [ANG-(1-7)] infusion reduced size attenuated ventricular dysfunction remodeling. We measured the effect of ANG-(1-7) on protein DNA synthesis in cultured neonatal rat myocytes assess role heptapeptide cell growth. significantly either fetal bovine serum- or endothelin-1-stimulated...

10.1152/ajpheart.00941.2004 article EN AJP Heart and Circulatory Physiology 2005-06-11

The degree of parasympathetic control heart rate was assessed by the abolition respiratory sinus arrhythmia with atropine. Peak-to-peak variations in periods (VHP) before atropine injection correlated significantly (r = 0.90, P less than 0.001) control, indicating that VHP alone may be used as a noninvasive indicator rate. Pharmacologic blockade beta-adrenergic supply separate group normal volunteers did not alter relationship between and condition experiment (complete rest quiet atmosphere)...

10.1152/ajpheart.1984.246.6.h838 article EN AJP Heart and Circulatory Physiology 1984-06-01

Although angiotensin II (Ang II) and the heptapeptide Ang-(1-7) differ by only one amino acid, two peptides produce different responses in vascular smooth muscle cells. We previously showed that Ang stimulated phosphoinositide hydrolysis, whereas released prostaglandins. now report differentially modulate rat aortic cell growth. inhibited [3H]thymidine incorporation response to stimulation fetal bovine serum, platelet-derived growth factor, or II. The reduction serum-stimulated thymidine...

10.1161/01.hyp.28.1.104 article EN Hypertension 1996-07-01

Angiotensin converting enzyme (ACE) inhibitors augment circulating levels of the vasodilator peptide angiotensin-(1–7) [Ang-(1–7)] in man and animals. Increased concentrations may contribute to antihypertensive effects associated with ACE inhibitors. The rise Ang-(1–7) following inhibition result from increased production or metabolism Ang-(1–7)-similar that observed for bradykinin. To address latter possibility, we determined whether is a substrate vitro. In pulmonary membrane preparation,...

10.1161/01.hyp.31.1.362 article EN Hypertension 1998-01-01

We have recently shown that hydrolysis of labeled angiotensin I in canine brainstem homogenate causes a rapid accumulation the heptapeptide angiotensin-(1-7) [Ang-(1-7)]. Although this fragment has no vasopressor activity, its consistent generation brain led us to study potential neurosecretory effects rat hypothalamo-neurohypophysial system (HNS) vitro. Ang-(1-7) or II (Ang II) was added HNS perifusate concentrations 0.04, 0.4, and 4 microM, release arginine vasopressin (AVP) during each...

10.1073/pnas.85.11.4095 article EN Proceedings of the National Academy of Sciences 1988-06-01

Background —Angiotensin II may contribute to atherogenesis by facilitating the proliferative and inflammatory response hypercholesterolemia. This study determined, in a primate model of diet-induced atherosclerosis, effect AT 1 blockade on fatty-streak formation, plasma lipids, surrogate markers vascular injury. Methods Results —Male cynomolgus monkeys fed diet containing 0.067 mg cholesterol/kJ for 20 weeks were given losartan (180 mg/d, n=6) or vehicle (n=8) 6 starting at week 12 dietary...

10.1161/01.cir.101.13.1586 article EN Circulation 2000-04-04

Recent studies have shown that angiotensin-(1–7) [Ang-(1–7)] interacts with kinins and augments bradykinin (BK)-induced vasodilator responses by an unknown mechanism. In this study, we evaluated whether the potentiation of BK-induced vasodilation Ang-(1–7) may be attributable to inhibition BK metabolism, release nitric oxide, or both. Isometric tension was measured in intact canine coronary artery rings suspended organ chambers. 125 I-[Tyr 0 ]-BK metabolism determined vascular assessing...

10.1161/01.hyp.29.1.394 article EN Hypertension 1997-01-01

This lecture summarizes the chronology and rationale that led to discovery of angiotensin-(1-7) as a hormone that, in its own right, opposes vasoconstrictor proliferative actions angiotensin II. The work discussed here additionally analyzes newest findings on angiotensin-converting enzyme 2, homologue efficiently hydrolyzes II into angiotensin-(1-7). Both components this system may significantly influence our future perspective role renin–angiotensin system, not just terms regulation...

10.1161/01.hyp.0000196268.08909.fb article EN Hypertension 2005-12-20

Angiotensin converting enzyme 2 (ACE2), a newly discovered member of the renin-angiotensin system (RAS), is potential therapeutic target for control cardiovascular disease owing to its key role in formation vasoprotective peptides from angiotensin II. The aim present study was evaluate whether overexpression ACE2 could protect heart II-induced hypertrophy and fibrosis. Lentiviral vector encoding mouse (lenti-mACE2) or GFP injected intracardially 5-day-old Sprague-Dawley rats. This resulted...

10.1113/expphysiol.2005.031096 article EN Experimental Physiology 2005-07-28

To evaluate the contribution of angiotensin-(1-7) [Ang-(1-7)] and prostaglandins to acute long-term antihypertensive actions captopril in mild-to-moderate essential hypertensive patients.Blood pressure, cardiac rate plasma concentrations angiotensin I (Ang I), II II), Ang-(1-7), prostaglandin E2 6-keto F1 alpha (the breakdown product prostacyclin) were determined peripheral venous blood 24 subjects before 3 h after administration 50 mg captopril. Eleven patients completed a 6-month treatment...

10.1097/00004872-199606000-00017 article EN Journal of Hypertension 1996-06-01
Coming Soon ...