Cardiovascular and Respiratory Pathology/Other Systemic Diseases

Vascular pathophysiology

Juan Ureña López
Juan Ureña López
IBiS
Campus Hospital Universitario Virgen del Rocío
Avda. Manuel Siurot, s/n.
41013 · Sevilla
Antonio Castellano Orozco
Antonio Castellano Orozco
IBiS
Campus Hospital Universitario Virgen del Rocío
Avda. Manuel Siurot, s/n.
41013 · Sevilla

Laboratory: 115

Juan Ureña López

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  1. Group members
  2. Research areas
  3. Publications

Group: Vascular pathophysiology

Directory
Group members Vascular pathophysiology
  • Castellano Orozco, Antonio.PhD in Biology. Associate Professor/Associate Researcher (University of Seville/HUVR).
  • Delgado de la Cuesta, Juan.FEA HUVR
  • Falcón Boyano, Débora.Degree in Biotechnology. PhD student.
  • Fierro Risco, Jesús.Dr. en Biología
  • González-Montelongo, Mª del Carmen.Doctora en Biología. Técnico.
  • Porras González, Cristina.Lda. en Biología. Técnico.
  • Ureña López, Juan.PhD in Physics. Professor/Associate Researcher (University of Seville/HUVR).
  • Varela Pérez, Lourdes María.Investigadora Postdoctoral US

Research areas

Our area of interest is the Molecular Pathophysiology of the Cardiovascular System. Our main objective is to study the mechanisms regulating vascular tone under physiological or pathophysiological situations. For this purpose we study the following aspects of vascular smooth muscle:

Mechanisms involved in cytosolic Ca2+ ([Ca2+]i)-dependent contraction.

Arterial contraction takes place in response to an increase in [Ca2+]i. This increase in [Ca2+]i can be produced by the influx of Ca2+ from the extracellular media or the release of Ca2+ from intracellular stores, such as the sarcoplasmic reticulum (SR). A classic route of entry for Ca2+ is via L-type Ca2+ channels on the plasma membrane. These channels can be used as therapeutic targets for the treatment of pathologies associated with vascular spasms, such as hypertension. On the other hand, the SR plays an important role because vasoactive agents such as NA, ATP, etc., can produce arterial contraction via Ca2+ release from the SR. In our laboratory we have described that L-type Ca2+ channels can induce the release of Ca2+ from the SR through a metabotropic route. One of our projects is to study the implications of this route in the control of vasospasm.

Mechanisms involved in Ca2+ sensitization-dependent contraction.

Arterial contraction can also be produced even though [Ca2+]i remains constant, i.e. contraction due to Ca2+ sensitization mechanisms. The two most important routes are related to RhoA/Rho kinase and protein kinase C. As this mechanism participates in pathophysiological conditions such as hypertension, coronary spasm, etc, we are interested in determining if the activation of the metabotropic route by Ca2+ channels indicated in the previous point can activate these sensitization pathways.

Regulation of the vascular tone by hypoxia.

Another topic of interest is the effect of hypoxia (acute and chronic) on voltage- and Ca2+-dependent potassium channels (Maxi-K channels), and on voltage-dependent Ca2+ channels (L or T types) of vascular smooth muscle, as well as to determine if there are differences in the responses of these channels to hypoxia in different vascular regions